Relation Results

Identifier	Residue	Sequence	Organism
SIGNOR-244622	Ser10	NVRVSNGsPSLERMD	Homo sapiens
pmid	sentence
10831586	Phosphorylation on ser-10 of kip1 is the major site of phosphorylation in resting cells, takes place at the g(0)-g1 phase and leads to protein stability.

Identifier	Residue	Sequence	Organism
SIGNOR-244517	Ser178	EENVSDGsPNAGSVE	Homo sapiens
pmid	sentence
10831586	Indeed, p27kip1 was phosphorylated by p42 mapk (erk2) in vitrothese results suggest that ser(10) is the major site of phosphorylation of p27(kip1) and that phosphorylation at this site, like that at thr(187), contributes to regulation of p27(kip1) stability.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, Integrin Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-244545	Ser1035	DHQTPPTsPVQGTTP	Homo sapiens
pmid	sentence
24089523	Histone deacetylase 6 (hdac6) is well known for its ability to promote cell migrationextracellular signal-regulated kinase (erk) phosphorylates histone deacetylase 6 (hdac6) at serine 1035 to stimulate cell migrationwe have identified two novel erk-mediated phosphorylation sites: threonine 1031 and serine 1035 in hdac6. Both sites were phosphorylated by erk1

Identifier	Residue	Sequence	Organism
SIGNOR-244549	Thr1031	ASSTDHQtPPTSPVQ	Homo sapiens
pmid	sentence
24089523	Histone deacetylase 6 (hdac6) is well known for its ability to promote cell migrationextracellular signal-regulated kinase (erk) phosphorylates histone deacetylase 6 (hdac6) at serine 1035 to stimulate cell migrationwe have identified two novel erk-mediated phosphorylation sites: threonine 1031 and serine 1035 in hdac6. Both sites were phosphorylated by erk1

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244647	Ser104	FPPLNSVsPSPLMLL	Homo sapiens	HeLa Cell
pmid	sentence
17615152	In several estrogen response element-containing genes, the s118a mutation strongly reduced induction by e(2), and u0126 did not further reduce expression. Here, we show that serines 104 (s104) and 106 (s106) are also phosphorylated by mapk in vitro and upon stimulation of mapk activity in vivo.Phosphorylation at serines 104 and 106 by erk1/2 mapk is important for estrogen receptor-alpha activity

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244651	Ser106	PLNSVSPsPLMLLHP	Homo sapiens	HeLa Cell
pmid	sentence
17615152	In several estrogen response element-containing genes, the s118a mutation strongly reduced induction by e(2), and u0126 did not further reduce expression. Here, we show that serines 104 (s104) and 106 (s106) are also phosphorylated by mapk in vitro and upon stimulation of mapk activity in vivo.Phosphorylation at serines 104 and 106 by erk1/2 mapk is important for estrogen receptor-alpha activity

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244655	Ser118	LHPPPQLsPFLQPHG	Homo sapiens	HeLa Cell
pmid	sentence
17615152	In several estrogen response element-containing genes, the s118a mutation strongly reduced induction by e(2), and u0126 did not further reduce expression. Here, we show that serines 104 (s104) and 106 (s106) are also phosphorylated by mapk in vitro and upon stimulation of mapk activity in vivo.

Publications:

3

Organism:

Homo Sapiens

Pathways:

Luminal Breast Cancer, Oxytocin signaling

Identifier	Residue	Sequence	Organism
SIGNOR-232236	Ser112	AIKVEPAsPPYYSEK	Homo sapiens
pmid	sentence
11733495	Moreover, the inhibition of erks 1 and 2 with a mek inhibitor, u1026, lead to an inhibition in the decay of ppargamma proteins, indicating that serine phosphorylation influences the degradation of ppargamma in fat cells.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Leptin Signaling, MTOR Signaling, Rett syndrome, Thyroid cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244580	Ser1132	TLPHGPRsASVSSIS	Chlorocebus aethiops	COS Cell
pmid	sentence
8816480	In this report, we describe the identification of five map kinase sites (s-1137, s-1167, s-1178, s-1193, and s-1197) on hsos1Replacing the MAP kinase phosphorylation sites with alanine residues results in an increase in the binding affinity of Grb2 to hSos1

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244584	Ser1167	ESAPAESsPSKIMSK	Chlorocebus aethiops	COS Cell
pmid	sentence
8816480	In this report, we describe the identification of five map kinase sites (s-1137, s-1167, s-1178, s-1193, and s-1197) on hsos1Replacing the MAP kinase phosphorylation sites with alanine residues results in an increase in the binding affinity of Grb2 to hSos1

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244588	Ser1197	KAYSPRYsISDRTSI	Chlorocebus aethiops	COS Cell
pmid	sentence
8816480	In this report, we describe the identification of five map kinase sites (s-1137, s-1167, s-1178, s-1193, and s-1197) on hsos1Replacing the MAP kinase phosphorylation sites with alanine residues results in an increase in the binding affinity of Grb2 to hSos1

Identifier	Residue	Organism
SIGNOR-244591		Homo sapiens
pmid	sentence
20724475	ERK activation was sufficient for the SOS1 phosphorylation and resulting inhibition of EGF-induced Ras activation. This result also showed that SOS1 could be phosphorylated by ERK in the absence of association with EGFR at the plasma membrane, which is a phosphotyrosine-dependent process.

Publications:

4

Organism:

Chlorocebus Aethiops, Homo Sapiens

Tissue:

Lung, Breast

Pathways:

Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Inhibition of Apoptosis, Integrin Signaling, Luminal Breast Cancer, Malignant Melanoma, Noonan syndrome, Non-small-cell lung cancer (NSCLC), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-244754	Ser117	YPSMPAFsPGPGIKE	Homo sapiens
pmid	sentence
10915800	Map kinases erk1/2 phosphorylate sterol regulatory element-binding protein (srebp)-1a at serine 117 in vitro. mutation of serine 117 to alanine abolished erk2-mediated phosphorylation in vitro and the map kinase-related transcriptional activation of srebp-1a by insulin and platelet-derived growth factor in vivo.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Insulin Signaling, MTOR Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-244743	Ser1178	IMSKHLDsPPAIPPR	Homo sapiens
pmid	sentence
20724475	ERK activation was sufficient for the SOS1 phosphorylation and resulting inhibition of EGF-induced Ras activation. This result also showed that SOS1 could be phosphorylated by ERK in the absence of association with EGFR at the plasma membrane, which is a phosphotyrosine-dependent process.

Identifier	Residue	Sequence	Organism
SIGNOR-244747	Ser1193	QPTSKAYsPRYSISD	Homo sapiens
pmid	sentence
20724475	ERK activation was sufficient for the SOS1 phosphorylation and resulting inhibition of EGF-induced Ras activation. This result also showed that SOS1 could be phosphorylated by ERK in the absence of association with EGFR at the plasma membrane, which is a phosphotyrosine-dependent process.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Inhibition of Apoptosis, Integrin Signaling, Luminal Breast Cancer, Malignant Melanoma, Noonan syndrome, Non-small-cell lung cancer (NSCLC), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-244618	Ser130	SGEQAEGsPGGPGDS	Homo sapiens
pmid	sentence
19364816	Extracellular signal-regulated kinase 2-dependent phosphorylation induces cytoplasmic localization and degradation of p21cip1.\|Phosphopeptide analysis of in vitro ERK2-phosphorylated p21(Cip1) revealed two phosphorylation sites, Thr57 and Ser130.

Identifier	Residue	Sequence	Organism
SIGNOR-244513	Thr57	NFDFVTEtPLEGDFA	Homo sapiens
pmid	sentence
19364816	We have shown that erk2 interacts with and phosphorylates p21cip1, promoting p21cip1_ubiquitination. We identified two erk2 phosphorylation sites, thr57 and ser130, in p21cip1_and showed that phosphorylation of these residues increases p21cip1_cytoplasmic distribution and proteasome-dependent degradation.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Rhabdomyosarcoma

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-274018	Ser14	TRVFKKSsPNCKLTV	Mus musculus	MEF Cell
pmid	sentence
26324936	ERK1/2-dependent βarr2 phosphorylation on S14 and T276 induces CXCR4 intracellular sequestration.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-274019	Thr276	FCKVYTItPLLSDNR	Mus musculus	MEF Cell
pmid	sentence
26324936	ERK1/2-dependent βarr2 phosphorylation on S14 and T276 induces CXCR4 intracellular sequestration.

Publications:

2

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244630	Ser1409	SAPEDPTsPKRKMRR	Homo sapiens	Melanoma Cell
pmid	sentence
21087211	Specifically, 14-3-3 binds to p90(rsk)-phosphorylated ser?_??_ Of capic?_A thereby modulating dna binding to its hmg (high-mobility group) box, whereas erk phosphorylations prevent binding of a c-terminal nls (nuclear localization sequence) to importin ?4 (kpna3)[...] These results suggest that erk phosphorylation of ser1382 and ser1409 masks the nls and prevents its binding to kpna3

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263064	Ser1448	TSRQSPAsPPPLGGG	Homo sapiens	HEK-293 Cell
pmid	sentence
20622900	HScrib is a substrate of ERK and PKA. Under normal growth conditions, hScrib is phosphorylated at S853, most likely by ERK, and at S1445 by PKA. Interestingly, stimulation of MAPK by osmotic stress results in a marked loss of phosphorylation at the PKA site S1445, but a concomitant increase in phosphorylation at S1448, presumably also by ERK. At present, we have no information as to what are the functional consequences of ERK or PKA phosphorylation of hScrib. However, we can speculate that this will most likely affect the ability of hScrib to interact with some of its cellular partners, and studies are currently in progress to investigate these aspects further.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263065	Ser853	LPLLPPEsPGPLRQR	Homo sapiens	HEK-293 Cell
pmid	sentence
20622900	HScrib is a substrate of ERK and PKA. Under normal growth conditions, hScrib is phosphorylated at S853, most likely by ERK, and at S1445 by PKA. Interestingly, stimulation of MAPK by osmotic stress results in a marked loss of phosphorylation at the PKA site S1445, but a concomitant increase in phosphorylation at S1448, presumably also by ERK. At present, we have no information as to what are the functional consequences of ERK or PKA phosphorylation of hScrib. However, we can speculate that this will most likely affect the ability of hScrib to interact with some of its cellular partners, and studies are currently in progress to investigate these aspects further.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-259919	Ser151	VARSNPKsPQKPIVR	Homo sapiens	Melanoma Cell
pmid	sentence
21478863	We show that overactivation of the MAPK pathway, induced by the oncogenic Ras in melanoma, induces constitutive phosphorylation of BRAF on Ser151 by ERK, which inhibits NRAS-BRAF interaction

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262966	Ser161	CEVGFIPsPVKLDSL	Chlorocebus aethiops	COS-7 Cell
pmid	sentence
16406008	Thus, Ser-447 on Ca(v)2.2 and Ser-161 and Ser-348 of Ca(v)beta1b appear to be both necessary and sufficient for ERK-dependent modulation of these channels. Together, our data strongly suggest that modulation of neuronal N-type VDCCs by ERK involves phosphorylation of Ca(v)2.2alpha1 and to a lesser extent possibly also Ca(v)beta subunits. On the basis of the evidence presented here, it is therefore suggested that ERK-dependent up-regulation of Cav2.2 channels is primarily mediated by phosphorylation of Ser-447 on the I–II loop of Cav2.2 and possibly also the two SP sites conserved on Cavβs.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262965	Ser348	IVYIKITsPKVLQRL	Chlorocebus aethiops	COS-7 Cell
pmid	sentence
16406008	Thus, Ser-447 on Ca(v)2.2 and Ser-161 and Ser-348 of Ca(v)beta1b appear to be both necessary and sufficient for ERK-dependent modulation of these channels. Together, our data strongly suggest that modulation of neuronal N-type VDCCs by ERK involves phosphorylation of Ca(v)2.2alpha1 and to a lesser extent possibly also Ca(v)beta subunits. On the basis of the evidence presented here, it is therefore suggested that ERK-dependent up-regulation of Cav2.2 channels is primarily mediated by phosphorylation of Ser-447 on the I–II loop of Cav2.2 and possibly also the two SP sites conserved on Cavβs.

Publications:

2

Organism:

Chlorocebus Aethiops

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262668	Ser173	MLETLSQsPPKGVTI	Mus musculus	K-562 Cell
pmid	sentence
17475908	All together, these data indicate that ERK-dependent phosphorylation of hnRNP-E2 at serines 173, 189, and 272, and threonine 213 is responsible for increased hnRNP-E2 protein stability in BCR/ABL-transformed cells.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism
SIGNOR-249575	Ser180	PGSSAPNsPMAMLTL	Homo sapiens
pmid	sentence
10673502	The current study reveals that c-kit signaling triggers two phosphorylation events on mi, which up-regulate transactivation potential yet simultaneously target mi for ubiquitin-dependent proteolysis. The specific activation/degradation signals derive from mapk/erk targeting of serine 73the results suggested that s1p reduced melanin synthesis via s1p(3) receptor-mediated erk and rsk-1 activation, and subsequent mitf dual phosphorylation and degradation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Malignant Melanoma

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-269088	Ser189 Ser283	SGILGITsPSADTNK DMKANLAsPTPADIG	Homo sapiens	RAMOS (RA.1) Cell
pmid	sentence
22593617	In this study, we demonstrated that PAX5 was phosphorylated by ERK1/2 in vitro and in vivo at serines 189 and 283. This phosphorylation attenuated the transcriptional repression of BLIMP1 by PAX5.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262968	Ser209	DMTLPGIsPPPEKQK	Homo sapiens	HeLa Cell
pmid	sentence
20551060	Phosphorylation and activation of cell division cycle associated 5 by mitogen-activated protein kinase play a crucial role in human lung carcinogenesis. Our data suggest that transactivation of CDCA5 and its phosphorylation at Ser209 by ERK play an important role in lung cancer proliferation, and that the selective suppression of the ERK-CDCA5 pathway could be a promising strategy for cancer therapy.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262969	Ser79	AVQSPRRsPRISFFL	Homo sapiens	HeLa Cell
pmid	sentence
20551060	Phosphorylation and activation of cell division cycle associated 5 by mitogen-activated protein kinase play a crucial role in human lung carcinogenesis. Our data suggest that transactivation of CDCA5 and its phosphorylation at Ser209 by ERK play an important role in lung cancer proliferation, and that the selective suppression of the ERK-CDCA5 pathway could be a promising strategy for cancer therapy.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-260084	Ser213	DNMIRRLsPAERAQG	Mus musculus	NIH-3T3 Cell
pmid	sentence
15060146	Leukemia-related transcription factor TEL is negatively regulated through extracellular signal-regulated kinase-induced phosphorylation. Overexpressed TEL becomes phosphorylated in vivo by activated ERK. TEL is also directly phosphorylated in vitro by ERK. The inducible phosphorylation sites are Ser(213) and Ser(257).

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, KIT in AML, AML_TRIPLETS, Triple mutant AML

Identifier	Residue	Sequence	Organism
SIGNOR-188131	Ser221	KVAAETQsPSLFGST	Homo sapiens
pmid	sentence
19767751	Erk phosphorylates nup50 at ser221 and ser315 erk phosphorylation of the fg repeat region of nup50 reduced its affinity for importin-beta family proteins, importin-beta and transportin.

Identifier	Residue	Sequence	Organism
SIGNOR-263043	Ser315	TQSKPVSsPFPTKPL	Homo sapiens
pmid	sentence
19767751	Erk phosphorylates nup50 at ser221 and ser315 phosphorylation of nup50 reduces affinity for importin-beta

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252741	Ser221	DHEKKAYsFCGTVEY	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252742	Ser363	TSRTPKDsPGIPPSA	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252746	Ser380	HQLFRGFsFVATGLM	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252744	Ser732	RRVRKLPsTTL	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252745	Thr359	DTEFTSRtPKDSPGI	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252743	Thr573	AENGLLMtPCYTANF	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Publications:

6

Organism:

Chlorocebus Aethiops

Pathways:

FLT3-ITD signaling, Leptin Signaling, PI3K/AKT Signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250553	Ser221	DHEKKAYsFCGTVEY	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250554	Ser363	TSRTPKDsPGIPPSA	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250555	Ser380	HQLFRGFsFVATGLM	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250556	Ser732	RRVRKLPsTTL	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250557	Thr359	DTEFTSRtPKDSPGI	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250558	Thr573	AENGLLMtPCYTANF	Chlorocebus aethiops	COS Cell
pmid	sentence
9430688	Several lines of evidence indicate that the mapkap-k1 isoforms are also activated by mapks in vivo via the ras-dependent protein kinase cascade that is triggered by growth factors or tumor-promoting phorbol esters, such as phorbol 12-myristate 13-acetate (pma). here we identify six sites in mapkap-k1a that become phosphorylated in transfected cos-1 cells. The inactive form of mapkap-k1a in unstimulated cells is partially phosphorylated at ser222 and ser733. Stimulation with phorbol 12-myristate 13-acetate induces the phosphorylation of thr360, ser364, thr574, and ser381 and increases the phosphorylation of ser222 and ser733.

Publications:

6

Organism:

Chlorocebus Aethiops

Pathways:

AMPK Signaling, FLT3-ITD signaling, Inhibition of Apoptosis, MTOR Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-118542	Ser225	VGSKTPAsPVVVQQG	Homo sapiens
pmid	sentence
14532121	Activation of sphingosine kinase 1 by erk1/2-mediated phosphorylation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-93554	Ser226	IDENCLLsPLAGEDD	in vitro
pmid	sentence
9199329	Cyclin-dependent kinase (CDK) and mitogen-activated protein kinase (MAPK) phosphorylate the rat glucocorticoid receptor in vitro at distinct sites that together correspond to the major phosphorylated receptor residues observed in vivo; MAPK phosphorylates receptor residues threonine 171 and serine 246, whereas multiple CDK complexes modify serines 224 and 232.\|MAPKs and CDKs exert opposite effects on receptor transcriptional enhancement. From our results, we speculate that activators of the MAPK pathway, such as growth factors, insulin, and certain oncoproteins, or inhibitors of CDK function, such as tumor growth factor beta (TGF_), p21, and p27, might attenuate receptor-induced transcrip- tional responses. In contrast, negative regulators of MAPK, such as pKA, as well as activators of CDK, such as the cyclins or CAKs, should potentiate receptor action.

Publications:

1

Organism:

In Vitro

Pathways:

Adipogenesis

Identifier	Residue	Sequence	Organism
SIGNOR-244692	Ser227	DHEKKAYsFCGTVEY	Homo sapiens
pmid	sentence
10980595	We have generated two monoclonal antibodies that recognize two phosphorylated sites, p-ser227 and p-thr577, in the n- and c-terminal kinase domains of rsk2, respectively. phosphorylation and activation of rsk2 by uv light involves the erk pathway

Identifier	Residue	Sequence	Organism
SIGNOR-244696	Thr577	AENGLLMtPCYTANF	Homo sapiens
pmid	sentence
10980595	We have generated two monoclonal antibodies that recognize two phosphorylated sites, p-ser227 and p-thr577, in the n- and c-terminal kinase domains of rsk2, respectively. phosphorylation and activation of rsk2 by uv light involves the erk pathway

Identifier	Residue	Organism
SIGNOR-244699		Homo sapiens
pmid	sentence
19282669	Erk-activates the rsk family of serine/threonine kinases,rsk1, rsk2, and rsk3.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-244533	Ser2279	PVQPNPMsPQQHMLP	Homo sapiens
pmid	sentence
17623675	Serine residues (ser-2279, ser-2315, and ser-2366) on the c terminus of p300 were the major signaling targets of egf. Furthermore, the c-terminal serine phosphorylation of p300 stimulated its histone acetyltransferase activity these results also constituted the first report identifying the unique p300 phosphorylation sites induced by erk2 in vivo.

Identifier	Residue	Sequence	Organism
SIGNOR-244634	Ser2315	RSPQPVPsPRPQSQP	Homo sapiens
pmid	sentence
17623675	Erk2-mediated c-terminal serine phosphorylation of p300 (ser-2279, ser-2315, and ser-2366) is vital to the regulation of epidermal growth factor-induced keratin 16 gene expression.

Identifier	Residue	Sequence	Organism
SIGNOR-244537	Ser2366	MEQGHFAsPDQNSML	Homo sapiens
pmid	sentence
17623675	Serine residues (ser-2279, ser-2315, and ser-2366) on the c terminus of p300 were the major signaling targets of egf. Furthermore, the c-terminal serine phosphorylation of p300 stimulated its histone acetyltransferase activity these results also constituted the first report identifying the unique p300 phosphorylation sites induced by erk2 in vivo.

Publications:

3

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, COVID-19 Causal Network

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-266376	Ser233	KNHIPVFsPALTDGS	Homo sapiens	HEK-293 Cell
pmid	sentence
32989218	The Ser-233 phosphorylation of DHPS by ERK1/2 is important for its function in cell proliferation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-244719	Ser245	NQSMDTGsPAELSPT	Homo sapiens
pmid	sentence
10197981	These results suggest that oncogenic ras, acting through mek1 and erk kinases, induces the phosphorylation of smad2 and smad3 .we show that phosphorylation of smad2, a mediator of the activin/transforming growth factor-beta signal, by activated extracellular signal-regulated kinase 1 (erk1) increases the amount of smad2 protein and leads to enhanced transcriptional activity

Identifier	Residue	Sequence	Organism
SIGNOR-244723	Ser250	TGSPAELsPTTLSPV	Homo sapiens
pmid	sentence
10197981	These results suggest that oncogenic ras, acting through mek1 and erk kinases, induces the phosphorylation of smad2 and smad3 .we show that phosphorylation of smad2, a mediator of the activin/transforming growth factor-beta signal, by activated extracellular signal-regulated kinase 1 (erk1) increases the amount of smad2 protein and leads to enhanced transcriptional activity

Identifier	Residue	Sequence	Organism
SIGNOR-244727	Ser255	ELSPTTLsPVNHSLD	Homo sapiens
pmid	sentence
10197981	These results suggest that oncogenic ras, acting through mek1 and erk kinases, induces the phosphorylation of smad2 and smad3 .we show that phosphorylation of smad2, a mediator of the activin/transforming growth factor-beta signal, by activated extracellular signal-regulated kinase 1 (erk1) increases the amount of smad2 protein and leads to enhanced transcriptional activity

Identifier	Residue	Sequence	Organism
SIGNOR-255020	Ser255	ELSPTTLsPVNHSLD	Homo sapiens
pmid	sentence
26194464	Taken together, ERK-mediated Smad2 linker phosphorylation is responsible for TH17 differentiation

Identifier	Residue	Sequence	Organism
SIGNOR-244731	Thr220	QSNYIPEtPPPGYIS	Homo sapiens
pmid	sentence
12193595	Phosphorylation of smad2 by erk increases its transcriptional activity /thr220 and ser245, ser250, and ser255 were possible phosphorylation sites. The phosphorylation of peak a peptide by erk1 is consistent with that prediction.

Identifier	Residue	Sequence	Organism
SIGNOR-244735	Thr8	MSSILPFtPPVVKRL	Homo sapiens
pmid	sentence
12193595	These results suggest that oncogenic ras, acting through mek1 and erk kinases, induces the phosphorylation of smad2 and smad3 .we show that phosphorylation of smad2, a mediator of the activin/transforming growth factor-beta signal, by activated extracellular signal-regulated kinase 1 (erk1) increases the amount of smad2 protein and leads to enhanced transcriptional activity

Publications:

6

Organism:

Homo Sapiens

Tissue:

Lung, Breast, Lung

Pathways:

Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244703	Ser249	DTRQIQPsPPWSYDQ	Homo sapiens	HEK-293T Cell
pmid	sentence
16046550	We have identified four phosphorylation sites on aml1c that are necessary for transcriptional activity of aml1c in k562 and 293t cells (27).4 mutation of these four sites (serine 276, serine 293, serine 303, and threonine 300) to alanine abolishes transcriptional activation, whereas mutation of these sites to aspartic acid (which mimics phosphorylation) results in a hyperactive protein.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244707	Ser266	QYLGSIAsPSVHPAT	Homo sapiens	HEK-293T Cell
pmid	sentence
16046550	We have identified four phosphorylation sites on aml1c that are necessary for transcriptional activity of aml1c in k562 and 293t cells (27).4 mutation of these four sites (serine 276, serine 293, serine 303, and threonine 300) to alanine abolishes transcriptional activation, whereas mutation of these sites to aspartic acid (which mimics phosphorylation) results in a hyperactive protein.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244715	Thr273	SPSVHPAtPISPGRA	Homo sapiens	HEK-293T Cell
pmid	sentence
16046550	We have identified four phosphorylation sites on aml1c that are necessary for transcriptional activity of aml1c in k562 and 293t cells (27).4 mutation of these four sites (serine 276, serine 293, serine 303, and threonine 300) to alanine abolishes transcriptional activation, whereas mutation of these sites to aspartic acid (which mimics phosphorylation) results in a hyperactive protein.

Publications:

3

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, KIT in AML, NPM1_new

Identifier	Residue	Sequence	Organism
SIGNOR-244573	Ser260	NMGLNPSsPNDPVTN	Homo sapiens
pmid	sentence
17604322	In colon cancer cells, the Ras/mitogen‐activated protein kinase (MAPK) pathway phosphorylates RXRalpha, which impairs its function as a heterodimeric partner for PPARgamma\|A point‐mutated RXRalpha T82A/S260A, which mimics the unphosphorylated form of RXRalpha, can form a heterodimer with PPARgamma and thereby activate target gene expression by binding to the PPRE

Identifier	Residue	Sequence	Organism
SIGNOR-262960	Thr82	HSMSVPTtPTLGFST	Homo sapiens
pmid	sentence
17604322	In colon cancer cells, the Ras/mitogen‐activated protein kinase (MAPK) pathway phosphorylates RXRalpha, which impairs its function as a heterodimeric partner for PPARgamma\|A point‐mutated RXRalpha T82A/S260A, which mimics the unphosphorylated form of RXRalpha, can form a heterodimer with PPARgamma and thereby activate target gene expression by binding to the PPRE

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia

Identifier	Residue	Sequence	Organism
SIGNOR-200953	Ser268	ASLSTTPsESPRAQA	Homo sapiens
pmid	sentence
23408424	Erk phosphorylates gephyrin at ser-268 to regulate size of gephyrin postsynaptic scaffold and strength of gabaergic transmission./ Ser-268 phosphorylation restricts gephyrin cluster size via calpain 1 proteolysis

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264443	Ser272	CSLERQLsLEQEVQQ	Homo sapiens	HeLa Cell
pmid	sentence
12670876	Intriguingly, a significant difference in the potency of nonredox-type inhibitors (but not of BWA4C) was determined between wild-type 5-LO and the mutant S271A/S663A-5-LO (lacking phosphorylation sites for ERK1/2 and MAPKAPK-2) in HeLa cells. Collectively, our data suggest that compared with Ca2+-mediated 5-LO product formation, enzyme activation involving 5-LO phosphorylation events specifically and strongly alters the susceptibility of 5-LO toward nonredox-type inhibitors in intact cells.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264442	Ser664	QLPYYYLsPDRIPNS	Homo sapiens	HeLa Cell
pmid	sentence
12670876	Intriguingly, a significant difference in the potency of nonredox-type inhibitors (but not of BWA4C) was determined between wild-type 5-LO and the mutant S271A/S663A-5-LO (lacking phosphorylation sites for ERK1/2 and MAPKAPK-2) in HeLa cells. Collectively, our data suggest that compared with Ca2+-mediated 5-LO product formation, enzyme activation involving 5-LO phosphorylation events specifically and strongly alters the susceptibility of 5-LO toward nonredox-type inhibitors in intact cells.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-260605	Ser274	DPLPGPGsPSHSAPD	Rattus norvegicus
pmid	sentence
18762583	Supporting the conclusion that phosphorylation of GRASP65 at Ser277 by ERK is critical for Golgi polarization. We have demonstrated a closely integrated mechanism in which Golgi remodeling by phosphorylation of GRASP65 acts as a negative regulator of Golgi and, surprisingly, centrosome orientation. Our data indicate that ERK phosphorylates GRASP65 in interphase cells, resulting in the loss of GRASP65 oligomerization and causing subsequent Golgi cisternal unstacking.

Publications:

1

Organism:

Rattus Norvegicus

Identifier	Residue	Sequence	Organism
SIGNOR-244711	Ser276	VHPATPIsPGRASGM	Homo sapiens
pmid	sentence
16046550	We have identified four phosphorylation sites on aml1c that are necessary for transcriptional activity of aml1c in k562 and 293t cells (27).4 mutation of these four sites (serine 276, serine 293, serine 303, and threonine 300) to alanine abolishes transcriptional activation, whereas mutation of these sites to aspartic acid (which mimics phosphorylation) results in a hyperactive protein.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, KIT in AML, NPM1_new

Identifier	Residue	Sequence	Organism
SIGNOR-244677	Ser289	RSHSESAsPSALSSS	Mus musculus
pmid	sentence
15664191	Here, we identify six residues of Raf-1 (S29, S43, S289, S296, S301, and S642) that become hyperphosphorylated in a manner coincident with Raf-1 inactivation. \| Five of the identified sites are proline-directed targets of activated ERK, and phosphorylation of all six sites requires MEK signaling, indicating a negative feedback mechanism. Hyperphosphorylation of these six sites inhibits the Ras/Raf-1 interaction and desensitizes Raf-1 to additional stimuli.\|FLAG-Raf-1 phosphorylated by activated ERK2

Identifier	Residue	Sequence	Organism
SIGNOR-244681	Ser296	SPSALSSsPNNLSPT	Mus musculus
pmid	sentence
15664191	Here, we identify six residues of Raf-1 (S29, S43, S289, S296, S301, and S642) that become hyperphosphorylated in a manner coincident with Raf-1 inactivation. \| Five of the identified sites are proline-directed targets of activated ERK, and phosphorylation of all six sites requires MEK signaling, indicating a negative feedback mechanism. Hyperphosphorylation of these six sites inhibits the Ras/Raf-1 interaction and desensitizes Raf-1 to additional stimuli.\|FLAG-Raf-1 phosphorylated by activated ERK2

Publications:

2

Organism:

Mus Musculus

Pathways:

Adipogenesis, COVID-19 Causal Network, Insulin Signaling, Integrin Signaling, Noonan syndrome, Oxytocin signaling, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-274070	Ser289	RSSTPLHsPSPIRVH	Homo sapiens	A-172 Cell
pmid	sentence
27659916	ERK-dependent phosphorylation of BIS following H2O2 treatment.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-274071	Thr285	GSPARSStPLHSPSP	Homo sapiens	A-172 Cell
pmid	sentence
27659916	ERK-dependent phosphorylation of BIS following H2O2 treatment.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-263068	Ser29	ATKAARKsAPSTGGV	Homo sapiens
pmid	sentence
11278789	In the present study, ERK1, ERK2, or p38 kinase strongly phosphorylated H3 at serine 28 in vitro. JNK1 or JNK2 was able also to phosphorylate H3 at serine 28 in vitro but to a lesser degree. Histone H3 phosphorylation is related closely to chromatin remodeling and chromosome condensation. H3 phosphorylation at serine 28 is coupled with mitotic chromosome condensation in diverse mammalian cell lines.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-244685	Ser301	SSSPNNLsPTGWSQP	Homo sapiens
pmid	sentence
16407412	Using mass spectrometry, we identified raf-1 phosphorylation on three sp motif sites: s289/s296/s301. These sites were phosphorylated by extracellular signal-regulated kinase (erk)-1 in vitro, and their phosphorylation in vivo was dependent on endogenous erk activity. Functionally, erk-1 expression sustains raf-1 activation in a manner dependent on raf-1 phosphorylation on the identified sites, and s289/296/301a substitution markedly decreases the in vivo activity of raf-1 s259a.

Identifier	Residue	Organism
SIGNOR-244688		Homo sapiens
pmid	sentence
9922370	Mapkerk1/2 is also able to phopshorylate the egf receptor, the ras exchange factor sos, mkkkraf1, and mkkmek1. The phosphorylation of each of these proteins by mapkerk1/2 is believed to reduce their catalytic activity

Publications:

2

Organism:

Homo Sapiens

Pathways:

Adipogenesis, COVID-19 Causal Network, Insulin Signaling, Integrin Signaling, Noonan syndrome, Oxytocin signaling, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Sequence	Organism
SIGNOR-252085	Ser324	RDLELPLsPSLLGGP	Homo sapiens
pmid	sentence
7889942	Erki phosphorylates five c-terminal sites in elk-i (s324, t336, s383, s389 and s422) with varying degrees of efficiency.

Identifier	Residue	Sequence	Organism
SIGNOR-252083	Ser383	IHFWSTLsPIAPRSP	Homo sapiens
pmid	sentence
7889942	Erki phosphorylates five c-terminal sites in elk-i (s324, t336, s383, s389 and s422) with varying degrees of efficiency.

Identifier	Residue	Sequence	Organism
SIGNOR-252086	Ser389	LSPIAPRsPAKLSFQ	Homo sapiens
pmid	sentence
7889942	Erki phosphorylates five c-terminal sites in elk-i (s324, t336, s383, s389 and s422) with varying degrees of efficiency.

Identifier	Residue	Sequence	Organism
SIGNOR-252084	Ser422	LSTPVVLsPGPQKP	Homo sapiens
pmid	sentence
7889942	Erki phosphorylates five c-terminal sites in elk-i (s324, t336, s383, s389 and s422) with varying degrees of efficiency.

Identifier	Residue	Sequence	Organism
SIGNOR-252082	Thr336	GGPGPERtPGSGSGS	Homo sapiens
pmid	sentence
7889942	Erki phosphorylates five c-terminal sites in elk-i (s324, t336, s383, s389 and s422) with varying degrees of efficiency.

Identifier	Residue	Organism
SIGNOR-252081		Homo sapiens
pmid	sentence
7618106	The tcf protein elk-1 is phosphorylated by the jnk and erk groups of mitogen-activated protein (map) kinases causing increased dna binding, ternary complex formation, and transcriptional activation

Publications:

6

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, Glioblastoma Multiforme, IL6 Signaling, Integrin Signaling, Noonan syndrome

Identifier	Residue	Sequence	Organism
SIGNOR-105754	Ser353	DSAIDTWsPSEWQMA	Homo sapiens
pmid	sentence
11259409	When subjected to phosphorylation by erk, the most efficient decrease in erk phosphorylation was observed with the s353a mutantamong the mechanisms underlying k protein ability to confer increased transcriptional output are interconversion of duplex and single-stranded dna (59) and association with the c/ebp_ (60), each of which could be better affected by the phosphorylated form of the k protein, which may increase affinity to associated proteins or dna.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-249572	Ser360	TEMDPTYsPAALPQS	Homo sapiens
pmid	sentence
18267068	Together, our in vivo and in vitro studies indicate that the pkc/c-raf/mek/erk pathway plays a major role in the s6k1 activation in hypertrophic cardiac growth.

Identifier	Residue	Sequence	Organism
SIGNOR-249573	Thr581	PDNQPLKtPCFTLHY	Homo sapiens
pmid	sentence
18267068	Together, our in vivo and in vitro studies indicate that the pkc/c-raf/mek/erk pathway plays a major role in the s6k1 activation in hypertrophic cardiac growth.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Malignant Melanoma

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244521	Ser362	ISSVPTPsPLGPLAG	Homo sapiens	Glioblastoma Cell
pmid	sentence
19941816	Erk2, which is activated by egfr signaling, directly binds to ck2alpha via the erk2 docking groove and phosphorylates ck2alpha primarily at t360/s362, subsequently enhancing ck2alpha activity

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244525	Thr360	SGISSVPtPSPLGPL	Homo sapiens	Glioblastoma Cell
pmid	sentence
19941816	Erk2, which is activated by egfr signaling, directly binds to ck2alpha via the erk2 docking groove and phosphorylates ck2alpha primarily at t360/s362, subsequently enhancing ck2alpha activity

Publications:

2

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263062	Ser362	PVHPKPLsPDSRASS	Homo sapiens	Prostate Cancer Cell Line
pmid	sentence
23188829	Mechanistic study revealed that EGF could activate the phosphorylation, ubiquitination, and degradation of EPLIN through an extracellular signal-regulated kinase 1/2 (ERK1/2)-dependent signaling cascade. Pharmacological inhibition of the ERK1/2 pathway effectively antagonized EGF-induced EPLIN degradation. Two serine residues, i.e. serine 362 and serine 604, were identified as putative ERK1/2 phosphorylation sites in human EPLIN, whose point mutation rendered resistance to EGF-induced protein turnover.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263063	Ser604	FQSTSVKsPKTVSPP	Homo sapiens	Prostate Cancer Cell Line
pmid	sentence
23188829	Mechanistic study revealed that EGF could activate the phosphorylation, ubiquitination, and degradation of EPLIN through an extracellular signal-regulated kinase 1/2 (ERK1/2)-dependent signaling cascade. Pharmacological inhibition of the ERK1/2 pathway effectively antagonized EGF-induced EPLIN degradation. Two serine residues, i.e. serine 362 and serine 604, were identified as putative ERK1/2 phosphorylation sites in human EPLIN, whose point mutation rendered resistance to EGF-induced protein turnover.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-262995	Ser362	AAAHRKGsSSNEPSS
pmid	sentence
16055710	Serine 374 and serine 362 are the primary sites targeted by Erk1/2 and the mitogen-activated protein kinase-activated kinases Rsk1/2 (12, 13, 37, 38, 41), respectively. Their phosphorylation leads to protein stabilization (3, 13, 20, 41). Threonine 325 and threonine 331 are secondary targets of Erk1/2; their modification occurs only when serines 362 and 374 are phosphorylated and Erk1/2 activation is sufficiently sustained (37, 38). This enhances the transcriptional activity of c-Fos

Identifier	Residue	Sequence	Organism
SIGNOR-251524	Ser374	PSSDSLSsPTLLAL	Homo sapiens
pmid	sentence
12972619	In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity.

Identifier	Residue	Sequence
SIGNOR-263010	Thr325	TELEPLCtPVVTCTP
pmid	sentence
16055710	Serine 374 and serine 362 are the primary sites targeted by Erk1/2 and the mitogen-activated protein kinase-activated kinases Rsk1/2 (12, 13, 37, 38, 41), respectively. Their phosphorylation leads to protein stabilization (3, 13, 20, 41). Threonine 325 and threonine 331 are secondary targets of Erk1/2; their modification occurs only when serines 362 and 374 are phosphorylated and Erk1/2 activation is sufficiently sustained (37, 38). This enhances the transcriptional activity of c-Fos

Identifier	Residue	Sequence	Organism
SIGNOR-251522	Thr325	TELEPLCtPVVTCTP	Homo sapiens
pmid	sentence
12972619	In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity.

Identifier	Residue	Sequence	Organism
SIGNOR-251523	Thr331	CTPVVTCtPSCTAYT	Homo sapiens
pmid	sentence
12972619	In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity.

Identifier	Residue	Sequence
SIGNOR-263009	Thr331	CTPVVTCtPSCTAYT
pmid	sentence
16055710	Serine 374 and serine 362 are the primary sites targeted by Erk1/2 and the mitogen-activated protein kinase-activated kinases Rsk1/2 (12, 13, 37, 38, 41), respectively. Their phosphorylation leads to protein stabilization (3, 13, 20, 41). Threonine 325 and threonine 331 are secondary targets of Erk1/2; their modification occurs only when serines 362 and 374 are phosphorylated and Erk1/2 activation is sufficiently sustained (37, 38). This enhances the transcriptional activity of c-Fos

Publications:

6

Organism:

, Homo Sapiens

Pathways:

Acute Myeloid Leukemia, EGFR Signaling, Leptin Signaling, T cell activation

Identifier	Residue	Sequence
SIGNOR-272239	Ser371	RIRRSGVsPLHLAAE
pmid	sentence
24044920	Indeed, using mass spectrometry, we showed for the first time that ASB2a is phosphorylated and that phosphorylation of serine-323 (Ser-323) of ASB2a is crucial for the targeting of the actin-binding protein filamin A (FLNa) to degradation. \|Moreover, inhibition of the extracellular signal-regulated kinases 1 and 2 (Erk1/2) activity reduced ASB2a-mediated FLNa degradation.

Publications:

1

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244669	Ser372	VAATPPPsTASAPAA	Homo sapiens	Neuron
pmid	sentence
16627622	Parp1 phosphorylation by erk1/2 is required for maximal parp-1 activation after dna damage. S372a and t373a mutations impaired parp-1 activation.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244673	Thr373	AATPPPStASAPAAV	Homo sapiens	Neuron
pmid	sentence
16627622	Parp1 phosphorylation by erk1/2 is required for maximal parp-1 activation after dna damage. S372a and t373a mutations impaired parp-1 activation.

Publications:

2

Organism:

Homo Sapiens

Tissue:

Brain

Pathways:

Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, Inhibition of Apoptosis

Identifier	Residue	Sequence	Organism
SIGNOR-252358	Ser374	PSSDSLSsPTLLAL	Homo sapiens
pmid	sentence
12972619	In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity.

Identifier	Residue	Sequence	Organism
SIGNOR-252359	Thr232	GGLPEVAtPESEEAF	Homo sapiens
pmid	sentence
7816602	Phosphorylation of the c-fos and c-jun hob1 motif stimulates its activation capacity here we show that the hob1-containing activation domain of c-fos is stimulated by ha-ras in vivo and phosphorylated by a map kinase family member in vitro and that mutating t232 to ala abolishes both functions.

Identifier	Residue	Sequence	Organism
SIGNOR-252357	Thr325	TELEPLCtPVVTCTP	Homo sapiens
pmid	sentence
12972619	In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity.

Identifier	Residue	Sequence	Organism
SIGNOR-252353	Thr331	CTPVVTCtPSCTAYT	Homo sapiens
pmid	sentence
12972619	In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity.

Publications:

4

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, B-cell activation, COVID-19 Causal Network, FLT3-ITD signaling, Hepatocellular Tumor, Luminal Breast Cancer, Leptin Signaling, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, T cell activation, Toll like receptors

Identifier	Residue	Sequence	Organism
SIGNOR-249574	Ser376	EKLFQGYsFVAPSIL	Homo sapiens
pmid	sentence
15568999	In the present study, we show that, in addition to being phosphorylated on Thr-581 and Ser-360 by ERK1/2 or p38, MSK1 can autophosphorylate on at least six sites: Ser-212, Ser-376, Ser-381, Ser-750, Ser-752 and Ser-758. Of these sites, the N-terminal T-loop residue Ser-212 and the 'hydrophobic motif' Ser-376 are phosphorylated by the C-terminal kinase domain of MSK1, and their phosphorylation is essential for the catalytic activity of the N-terminal kinase domain of MSK1

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Malignant Melanoma

Identifier	Residue	Sequence	Organism
SIGNOR-244509	Ser387	YLEMDLSsPQTRYIP	Homo sapiens
pmid	sentence
24342355	We demonstrate that perk 1/2 can phosphorylate pro-caspase-8 at s387 by knocking-down the endogenous pro-caspase-8 using rnai and replacing it with its non-phosphorylatable counterpart (s387a), a significant increase in caspase-8 activity

Publications:

1

Organism:

Homo Sapiens

Tissue:

Breast

Pathways:

COVID-19 Causal Network

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262980	Ser416	GFPSKTDsPSCEYSR	Homo sapiens	HEK-293 Cell
pmid	sentence
27846390	Here we show that ERK suppresses pre-miRNA export from the nucleus through phosphorylation of exportin-5 (XPO5) at T345/S416/S497. After phosphorylation by ERK, conformation of XPO5 is altered by prolyl isomerase Pin1, resulting in reduction of pre-miRNA loading.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262983	Ser497	GSLCSVFsPSFVQWE	Homo sapiens	HEK-293 Cell
pmid	sentence
27846390	Here we show that ERK suppresses pre-miRNA export from the nucleus through phosphorylation of exportin-5 (XPO5) at T345/S416/S497. After phosphorylation by ERK, conformation of XPO5 is altered by prolyl isomerase Pin1, resulting in reduction of pre-miRNA loading.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262986	Thr345	GADSDVEtPSNFGKY	Homo sapiens	HEK-293 Cell
pmid	sentence
27846390	Here we show that ERK suppresses pre-miRNA export from the nucleus through phosphorylation of exportin-5 (XPO5) at T345/S416/S497. After phosphorylation by ERK, conformation of XPO5 is altered by prolyl isomerase Pin1, resulting in reduction of pre-miRNA loading.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-244595	Ser428	SSKIRRLsACKQQ	Homo sapiens
pmid	sentence
25846811	Directly and/or through the activation of p90RSK, ERK phosphorylates LKB-1 at Ser325 and Ser428. The phosphorylation of LKB-1 causes the dissociation of LKB-1 from AMPK, resulting in the impaired activation of AMPK.

Publications:

1

Organism:

Homo Sapiens

Pathways:

AMPK Signaling, FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-265953	Ser43	RNPEAALsPTFRSDS	Homo sapiens	HEK-293 Cell
pmid	sentence
33217317	Mass spectrometry analysis showed that ERK phosphorylates METTL3 at three highly conserved residues: S43, S50, and S525 (Figures 2D and 2E). Mutational analysis further confirmed these three sites as main ERK phosphorylation sites (Figure 2F). Phosphorylation of METTL3 increases interaction with USP5, decreasing ubiquitination to stabilize the m6 A methyltransferase complex.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-265951	Ser50	SPTFRSDsPVPTAPT	Homo sapiens	HEK-293 Cell
pmid	sentence
33217317	Mass spectrometry analysis showed that ERK phosphorylates METTL3 at three highly conserved residues: S43, S50, and S525 (Figures 2D and 2E). Mutational analysis further confirmed these three sites as main ERK phosphorylation sites (Figure 2F). Phosphorylation of METTL3 increases interaction with USP5, decreasing ubiquitination to stabilize the m6 A methyltransferase complex.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-265952	Ser525	YGMIERLsPGTRKIE	Homo sapiens	HEK-293 Cell
pmid	sentence
33217317	Mass spectrometry analysis showed that ERK phosphorylates METTL3 at three highly conserved residues: S43, S50, and S525 (Figures 2D and 2E). Mutational analysis further confirmed these three sites as main ERK phosphorylation sites (Figure 2F). Phosphorylation of METTL3 increases interaction with USP5, decreasing ubiquitination to stabilize the m6 A methyltransferase complex.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-262967	Ser446	ADLCAVGsPFARASL	Chlorocebus aethiops
pmid	sentence
16406008	Thus, Ser-447 on Ca(v)2.2 and Ser-161 and Ser-348 of Ca(v)beta1b appear to be both necessary and sufficient for ERK-dependent modulation of these channels. Together, our data strongly suggest that modulation of neuronal N-type VDCCs by ERK involves phosphorylation of Ca(v)2.2alpha1 and to a lesser extent possibly also Ca(v)beta subunits. On the basis of the evidence presented here, it is therefore suggested that ERK-dependent up-regulation of Cav2.2 channels is primarily mediated by phosphorylation of Ser-447 on the I–II loop of Cav2.2 and possibly also the two SP sites conserved on Cavβs.

Publications:

1

Organism:

Chlorocebus Aethiops

Identifier	Residue	Sequence	Organism
SIGNOR-129188	Ser454	YVPMNPNsPPRQHSS	Homo sapiens
pmid	sentence
15379552	Erk phosphorylation enhances hgf-dependent gab1/pi3k but inhibits egf-dependent gab1/pi3k association and activation implicates that mapk activation provides another specific regulatory mechanism which can result in divergent effects for distinct rtks.we identified four serine and two threonine residues that are phosphorylated by erk in vitro. Five of these phosphorylation sites (t312, s454, t476, s581, s597)

Identifier	Residue	Sequence	Organism
SIGNOR-129192	Ser597	VPMNPNLsSEDPNLF	Homo sapiens
pmid	sentence
15379552	Erk phosphorylation enhances hgf-dependent gab1/pi3k but inhibits egf-dependent gab1/pi3k association and activation implicates that mapk activation provides another specific regulatory mechanism which can result in divergent effects for distinct rtks.we identified four serine and two threonine residues that are phosphorylated by erk in vitro. Five of these phosphorylation sites (t312, s454, t476, s581, s597)

Identifier	Residue	Sequence	Organism
SIGNOR-129196	Thr312	ISYDIPPtPGNTYQI	Homo sapiens
pmid	sentence
15379552	Erk phosphorylation enhances hgf-dependent gab1/pi3k but inhibits egf-dependent gab1/pi3k association and activation implicates that mapk activation provides another specific regulatory mechanism which can result in divergent effects for distinct rtks.we identified four serine and two threonine residues that are phosphorylated by erk in vitro. Five of these phosphorylation sites (t312, s454, t476, s581, s597)

Identifier	Residue	Sequence	Organism
SIGNOR-129200	Thr476	EANYVPMtPGTFDFS	Homo sapiens
pmid	sentence
15379552	Erk phosphorylation enhances hgf-dependent gab1/pi3k but inhibits egf-dependent gab1/pi3k association and activation implicates that mapk activation provides another specific regulatory mechanism which can result in divergent effects for distinct rtks.we identified four serine and two threonine residues that are phosphorylated by erk in vitro. Five of these phosphorylation sites (t312, s454, t476, s581, s597)

Publications:

4

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, Hepatocellular Tumor, Noonan syndrome, PI3K/AKT Signaling, Rhabdomyosarcoma

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244606	Ser516	VSRVPYPsPTCVKSE	Homo sapiens	Prostate Gland Cancer Cell
pmid	sentence
18511414	Map kinase-dependent phosphorylation at ar ser-515 was supported by the decrease in intensity of the slower migrating 23-kda band after treatment with both egf and increasing concentrations of the map kinase inhibitor, u0126

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244553	Ser523	GVSDVPTsPTLQRPT	Chlorocebus aethiops	COS Cell
pmid	sentence
16705159	We hypothesize that phosphorylation of ser523 in jak2 by erks 1 and/or 2 or other as-yet-unidentified kinases acts in a negative feedback manner

Publications:

1

Organism:

Chlorocebus Aethiops

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, EGFR Signaling, Leptin Signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244569	Ser532	KIKQEVEsPTDKSGN	Homo sapiens	JURKAT Cell
pmid	sentence
8960373	Functional analysis of phosphorylation at serine 532 of human c-myb by map kinase. expression of a polypeptide containing the c-myb c-terminal domain stimulated c-myb activity. This effect is reduced upon mapk-dependent phosphorylation of serine 532. Our data suggest that the mapk-dependent state of phosphorylation modifies the cellular function of c-myb by modulating its interaction with a putative inhibitory factor

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-268341	Ser537	DNSMSVPsPTSATKT	Mus musculus	Oocyte
pmid	sentence
34048556	Once an oocyte resumes meiosis, activated CDK1 and ERK1/2 cooperatively mediate the phosphorylation of three serine residues of PAPalpha, 537, 545 and 558, thereby leading to increased activity.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-268342	Ser545	PTSATKTsPLNSSGS	Mus musculus	Oocyte
pmid	sentence
34048556	Once an oocyte resumes meiosis, activated CDK1 and ERK1/2 cooperatively mediate the phosphorylation of three serine residues of PAPalpha, 537, 545 and 558, thereby leading to increased activity.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-268343	Ser558	GSSQGRNsPAPAVTA	Mus musculus	Oocyte
pmid	sentence
34048556	Once an oocyte resumes meiosis, activated CDK1 and ERK1/2 cooperatively mediate the phosphorylation of three serine residues of PAPalpha, 537, 545 and 558, thereby leading to increased activity.

Publications:

3

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249455	Ser540	KVMARSLsPPPELEE	Mus musculus	NIH-3T3 Cell
pmid	sentence
15851026	Here, we show that Erk may play a critical role in TSC progression through posttranslational inactivation of TSC2. Erk-dependent phosphorylation leads to TSC1-TSC2 dissociation and markedly impairs TSC2 ability to inhibit mTOR signaling, cell proliferation, and oncogenic transformation. \|Serine to alanine substitution at S664 or double S664A/S540A mutagenesis resulted in a marked reduction in TSC2 phosphorylation to a similar extent. In contrast, S540A substitution only moderately impaired TSC2 phosphorylation (Figure 3D), corroborating the notion that in vivo S664 is the most relevant residue for Erk-mediated phosphorylation.

Identifier	Residue	Organism	Cell Line
SIGNOR-244602		Homo sapiens	Breast Cancer Cell, Prostate Gland Cancer Cell, Leukemia Cell, Glioblastoma Cell
pmid	sentence
19188143	Phosphorylation of tsc2 (by akt and erk;refs. 28, 29) and tsc1(by ikkbeta;ref. 30) results in the disruption of the tsc1/2 complex, and thereby activates the oncogenic mtor signaling contributing to tumor progression

Publications:

2

Organism:

Mus Musculus, Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-275407	Ser616	PIPIMPAsPQKGHAV	Homo sapiens	HEK-293 Cell
pmid	sentence
25658205	Here, we show that expression of oncogenic Ras or direct activation of the MAPK pathway leads to increased mitochondrial fragmentation and that blocking this phenotype, through knockdown of the mitochondrial fission-mediating GTPase Drp1, inhibits tumor growth. This fission is driven by Erk2-mediated phosphorylation of Drp1 on Serine 616, and both this phosphorylation and mitochondrial fragmentation are increased in human pancreatic cancer.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252079	Ser62	LLPTPPLsPSRRSGL	Rattus norvegicus	Embryonic Fibroblast
pmid	sentence
11018017	Phosphorylation of Ser 62 is required for Ras-induced stabilization of Myc, likely mediated through the action of ERK.

Publications:

1

Organism:

Rattus Norvegicus

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, FLT3-ITD in AML, FLT3-ITD signaling, Hepatocellular Tumor, Nucleotide Biosynthesis, Triple mutant AML, NPM1_new, Rhabdomyosarcoma, Thyroid cancer, WNT/FLT3

Identifier	Residue	Sequence	Organism
SIGNOR-244765	Ser664	KKTSGPLsPPTGPPG	Homo sapiens
pmid	sentence
15851026	Here, we show that erk may play a critical role in tsc progression through posttranslational inactivation of tsc2. s664 is the primary erk phosphorylation site on tsc2 in vitro and in vivo

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244501	Ser70	RDPVARTsPLQTPAA	Chlorocebus aethiops	COS Cell
pmid	sentence
10677502	Erk1 and erk2 directly phosphorylate bcl2 exclusively at ser-70.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244505	Ser87	AAAGPALsPVPPVVH	Homo sapiens	HeLa Cell
pmid	sentence
10669763	The results of this study reveal the following novel findings: destruction of the three putative MAP kinase sites at positions 56, 74, and 87 results in ubiquitination and subsequent degradation of the protein. Progressive inactivation of these MAP kinase sites revealed that Bcl-2 stability is mainly regulated by phosphorylation at Thr74 and Ser87, with Ser87 phosphorylation playing a predominant role. TNF-α or the MAP kinase-specific inhibitor PD98059 diminishes Ser87 phosphorylation of Bcl-2 in vivo, while activated ERK2 induces phosphorylation of Bcl-2 in vivo and in vitro.

Identifier	Residue	Sequence	Organism
SIGNOR-244610	Thr56	FSSQPGHtPHPAASR	Homo sapiens
pmid	sentence
10669763	The results of this study reveal the following novel findings: destruction of the three putative MAP kinase sites at positions 56, 74, and 87 results in ubiquitination and subsequent degradation of the protein. Progressive inactivation of these MAP kinase sites revealed that Bcl-2 stability is mainly regulated by phosphorylation at Thr74 and Ser87.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244494	Thr74	ARTSPLQtPAAPGAA	Homo sapiens	HeLa Cell
pmid	sentence
10669763	The results of this study reveal the following novel findings: destruction of the three putative MAP kinase sites at positions 56, 74, and 87 results in ubiquitination and subsequent degradation of the protein. Progressive inactivation of these MAP kinase sites revealed that Bcl-2 stability is mainly regulated by phosphorylation at Thr74 and Ser87, with Ser87 phosphorylation playing a predominant role. TNF-α or the MAP kinase-specific inhibitor PD98059 diminishes Ser87 phosphorylation of Bcl-2 in vivo, while activated ERK2 induces phosphorylation of Bcl-2 in vivo and in vitro.

Publications:

4

Organism:

Chlorocebus Aethiops, Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, COVID-19 Causal Network, Colorectal Carcinoma, FLT3-ITD signaling, Inhibition of Apoptosis, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), SARS-CoV MAPK PERTURBATION

Identifier	Residue	Sequence	Organism
SIGNOR-263056	Ser734	SLKGKPLsEAIHLLQ	in vitro
pmid	sentence
11301320	Here we show that epidermal growth factor regulates the activities of the p160 GRIP1 through the extracellular signal-regulated kinase (ERK) family of mitogen-activated protein kinases. ERKs phosphorylate GRIP1 at a specific site, Ser-736, the integrity of which is required for full growth factor induction of GRIP1 transcriptional activation and coactivator function.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-244541	Ser777	SMPLDQYsPSFPDTR	Homo sapiens
pmid	sentence
23405013	Erk-mediated phosphorylation of fibroblast growth factor receptor 1 on ser777 inhibits signaling

Publications:

1

Organism:

Homo Sapiens

Pathways:

Luminal Breast Cancer

Identifier	Residue	Sequence	Organism
SIGNOR-174878	Ser863	LTQSAPAsPTNKGVH	Homo sapiens
pmid	sentence
21071439	We found three proline-directed residues within raptor, ser(8), ser(696), and ser(863), which are directly phosphorylated by erk1/2. Expression of phosphorylation-deficient alleles of raptor revealed that phosphorylation of these sites by erk1/2 normally promotes mtorc1 activity and signaling to downstream substrates, such as 4e-bp1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

MTOR Signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262522	Ser9	SGRPRTTsFAESCKP	Mus musculus	MEF Cell
pmid	sentence
28646232	We demonstrate that insulin-mediated activation of ERK1/2 results in phosphorylation of GSK3β at S9 independently of Akt/mTORC1 activity in Tsc2 null mouse embryonic fibroblasts. In addition, we show that inhibition of ERK1/2 rescues GSK3β activity and restores protein synthesis in Tsc2 −/− MEFs to normal levels

Publications:

1

Organism:

Mus Musculus

Pathways:

Adipogenesis, Acute Myeloid Leukemia, AML_TRIPLETS, FLT3-ITD signaling, Insulin Signaling, MTOR Signaling, Triple mutant AML, PI3K/AKT Signaling, WNT/FLT3

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-272330	Thr157	ARLVPIDtPNHLQRQ	Homo sapiens	KYSE-30 Cell
pmid	sentence
28716524	HECTD3 binds and ubiquitinates caspase-9.Phosphorylation of HECTD3 by ERK is required for the association of HECTD3 and caspase-9. HECTD3 suppressing caspase-9 activation is dependent on T157 phosphorylation by ERK.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-273669	Thr159	GHRATALtPDSCPLP	in vitro
pmid	sentence
31121283	The luminescence obtained in the kinase assay with FLAG-ShcD as substrate was significantly different to that with FLAG peptide suggesting that ShcD is a direct substrate of ERK (Fig. 2C).Furthermore, Thr159 was mutated to either alanine (A) or glutamic acid (E) to study whether the threonine phosphorylation state influences the ShcD/ERK interaction. Introducing the T159E mutation obliterated the ShcD/ERK interaction.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-244614	Thr160	GVPVRTYtHEVVTLW	Homo sapiens
pmid	sentence
12359725	In addition to its role in stimulating cyclin d1 expression and nuclear translocation of cdk2, erk regulates thr-160 phosphorylation of cdk2-cyclin e.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis

Identifier	Residue	Sequence	Organism
SIGNOR-244565	Thr207	FLTEYVAtRWYRAPE	Homo sapiens
pmid	sentence
19060905	Here we show that autophosphorylation of erk1/2 on thr188 directs erk1/2 to phosphorylate nuclear targets known to cause cardiac hypertrophy.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Heart

Identifier	Residue	Sequence	Organism
SIGNOR-251525	Thr232	GGLPEVAtPESEEAF	Homo sapiens
pmid	sentence
7816602	Phosphorylation of the c-fos and c-jun hob1 motif stimulates its activation capacity here we show that the hob1-containing activation domain of c-fos is stimulated by ha-ras in vivo and phosphorylated by a map kinase family member in vitro and that mutating t232 to ala abolishes both functions.

Identifier	Residue	Organism	Cell Line
SIGNOR-260762		Homo sapiens	HuH-7 Cell
pmid	sentence
21561061	3b Augments c-Fos Levels by Activating the ERK Pathway. \| Higher c-Fos levels were observed in 3b-expressing cells than in GFP-expressing control cells

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, EGFR Signaling, Leptin Signaling, T cell activation

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-238303	Thr235	SSSSPPGtPSPADAK	Homo sapiens	Lung Cancer Cell
pmid	sentence
19723873	Phosphorylation of cebpb at thr(235) peaked at 16 hours in il-1beta-stimulated cells. The mek inhibitor u0126 inhibited this phosphorylation and reduced mmp-1 gene induction.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Acute Myeloid Leukemia, FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-253014	Thr250	NSCTPITtPELTTPC	Homo sapiens	MCF-7 Cell
pmid	sentence
17130135	We generated a phosphospecific antibody to Thr(P)-214 in the T-loop of MNKs and found that phosphorylations of both Thr-209 and Thr-214 in human MNK1 are required for activation

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-253015	Thr255	ITTPELTtPCGSAEY	Homo sapiens	MCF-7 Cell
pmid	sentence
17130135	We generated a phosphospecific antibody to Thr(P)-214 in the T-loop of MNKs and found that phosphorylations of both Thr-209 and Thr-214 in human MNK1 are required for activation

Identifier	Residue	Organism
SIGNOR-253013		in vitro
pmid	sentence
9155018	These results indicate that MNK1 is a novel class of protein kinase that is activated through both the ERK and p38 MAP kinase signaling pathways

Publications:

3

Organism:

Homo Sapiens, In Vitro

Pathways:

PI3K/AKT Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-244739	Thr277	GSRTAPYtPNLPHHQ	Homo sapiens
pmid	sentence
12801888	Our results suggest that map kinase can phosphorylate thr276 of smad4 and that phosphorylation can lead to enhanced tgf-beta-induced nuclear accumulation and, as a consequence, enhanced transcriptional activity of smad4.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Colorectal Carcinoma, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244557	Thr292	ETPPRPRtPGRPLSS	Chlorocebus aethiops	COS Cell
pmid	sentence
14993270	We propose that activation of erk during adhesion creates a feedback system in which erk phosphorylates mek1 on t292, and this in turn blocks additional s298 phosphorylation in response to integrin signaling.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244561	Thr386	IGLNQPStPTHAAGV	Homo sapiens	HEK-293 Cell
pmid	sentence
10567369	An ERK2-binding site at the N terminus of MEK1 was reported to mediate their stable association. We examined the importance of this binding site in the feedback phosphorylation of mek1 on thr(292) and thr(386) by erk2

Publications:

2

Organism:

Chlorocebus Aethiops, Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-266203	Thr337	VKSFSRRtPNSSSYC	Homo sapiens	HeLa Cell
pmid	sentence
26080397	ERK-MAPK pathway that regulates alternative splicing facilitates ERK-1/2-mediated phosphorylation of SMAR1 at threonines 345 and 360 and localizes SMAR1 to the cytoplasm, preventing its interaction with Sam68.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-266377	Thr337	VKSFSRRtPNSSSYC	Homo sapiens	HeLa Cell
pmid	sentence
26080397	ERK-MAPK pathway that regulates alternative splicing facilitates ERK-1/2-mediated phosphorylation of SMAR1 at threonines 345 and 360 and localizes SMAR1 to the cytoplasm, preventing its interaction with Sam68.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-266204	Thr352	PSEPMMStPPPASEL	Homo sapiens	HeLa Cell
pmid	sentence
26080397	ERK-MAPK pathway that regulates alternative splicing facilitates ERK-1/2-mediated phosphorylation of SMAR1 at threonines 345 and 360 and localizes SMAR1 to the cytoplasm, preventing its interaction with Sam68.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-266378	Thr352	PSEPMMStPPPASEL	Homo sapiens	HeLa Cell
pmid	sentence
26080397	ERK-MAPK pathway that regulates alternative splicing facilitates ERK-1/2-mediated phosphorylation of SMAR1 at threonines 345 and 360 and localizes SMAR1 to the cytoplasm, preventing its interaction with Sam68.

Publications:

4

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-170339	Thr401	STTGLSAtPPASLPG	Homo sapiens
pmid	sentence
21135229	We show that b-raf is a calcineurin substrate;among calcineurin target residues on b-raf is t401, a site of negative feedback phosphorylation by erk1/2. Blocking calcineurin activity in _ cells prevents dephosphorylation of b-raf t401 and decreases b-raf and erk1/2 activities.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-267441	Thr456	KVYFLPItPHYVTQV	in vitro
pmid	sentence
17485345	The multifunctional protein CAD initiates de novo pyrimidine biosynthesis in mammalian cells. CAD is activated by MAP kinase (Erk1/2) just prior to the S phase of the cell cycle, when the demand for pyrimidine nucleotides is greatest, and down-regulated as the cells emerge from S phase by protein kinase A (PKA) phosphorylation. MAP kinase phosphorylates Thr456, while PKA phosphorylates Ser1406 and Ser1859, although only Ser1406 is involved in regulation.

Publications:

1

Organism:

In Vitro

Pathways:

Nucleotide Biosynthesis

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-274134	Thr562	LPRSLASTPTAPTTP	Mus musculus	MEF Cell
pmid	sentence
25801171	Finally, in Mfn1 -/- cells re-expressing the MFN1 T562A mutant, phosphorylation was undetectable even in the presence of EGF. Taken together, these data indicate that ERK phosphorylates MFN1 at T562.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism
SIGNOR-260755	Thr69	SVIVADQtPTPTRFL	Homo sapiens
pmid	sentence
20068231	Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Sequence	Organism
SIGNOR-244529	Thr693	RELVEPLtPSGEAPN	Homo sapiens
pmid	sentence
10816576	It is likely that the map2 and ert kinases account for the phosphorylation of the egf receptor at thr669 (egf receptor (krel veplt669psgeapnqallr)) observed in cultured cells.Phosphorylation at ser-695 is partial and occurs only if thr-693 is phosphorylated. Phosphorylation at thr-678 and thr-693 by prkd1 inhibits egf-induced mapk8/jnk1 activation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, COVID-19 Causal Network, EGFR Signaling, FLT3-ITD in AML, Glioblastoma Multiforme, Hepatocellular Tumor, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Sequence	Organism
SIGNOR-89614	Thr735	KPFPAPQtPGRLQPA	Homo sapiens
pmid	sentence
12058067	We report that the cytosolic tail of the tumor necrosis factor alpha-converting enzyme (tace) is phosphorylated by erk at threonine 735.These results demonstrate that secretases are able to discriminate between the different stimuli that trigger membrane protein ectodomain cleavage and indicate that phosphorylation by mapks may regulate the proteolytic function of membrane secretases.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263057	Thr789	PPAPPPPtPLEESTP	Chlorocebus aethiops	COS-7 Cell
pmid	sentence
16024771	CdGAP interacts with and is phosphorylated by ERK-1 and RSK-1 in vitro. A putative DEF (docking for ERK FXFP) domain located in the proline-rich region of CdGAP is required for efficient binding and phosphorylation by ERK1/2. We identify Thr776 as an in vivo target site of ERK1/2 and as an important regulatory site of CdGAP activity. Together, these data suggest that CdGAP is a novel substrate of ERK1/2 and mediates cross talk between the Ras/mitogen-activated protein kinase pathway and regulation of Rac1 activity.

Publications:

1

Organism:

Chlorocebus Aethiops

Identifier	Residue	Organism
SIGNOR-255022		Homo sapiens
pmid	sentence
16306329	Upon formation of the IL-6/IL-6Ralpha/gp130 hexameric signaling complex, two distinct signaling pathways are activated: 1) Janus kinase (JAK)/signal transducers and activator of transcription (STAT) and 2) the Src homology 2-containing tyrosine phosphatase (SHP-2)/extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathways

Publications:

1

Organism:

Homo Sapiens

Pathways:

IL6 Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-264978		Mus musculus	Neuron
pmid	sentence
12676795	Activation of the Ras-MAPK/Erk signaling cascade is essential for neurotrophin-promoted differentiation of neurons and PC12 cells.

Publications:

1

Organism:

Mus Musculus

Pathways:

Oxytocin signaling, Rett syndrome

Identifier	Residue	Organism	Cell Line
SIGNOR-262211		Homo sapiens	A-549 Cell
pmid	sentence
27995049	We also investigated the potential regulation of cancer-associated signaling pathways by Anxa3 through screening for the altered expression of some common signaling molecules after Anxa3 downregulation. Decreased phosphorylation of MEK1/2, ERK1/2, Akt, and IκBα was detected after downregulating Anxa3 expression in A549 cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270199		Homo sapiens
pmid	sentence
12356758	Phosphorylation of transcriptional coactivator peroxisome proliferator-activated receptor (ppar)-binding protein (pbp). Stimulation of transcriptional regulation by mitogen-activated protein kinase

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-263507		Homo sapiens
pmid	sentence
11085989	We also show for the first time that leptin rapidly stimulates the mRNA expression of the zinc finger transcription factor, Egr-1, in the hypothalamus of mice. Our transfection results suggest that this regulation by leptin occurs by activation of theegr-1 promoter via activation of SHP-2 and of the ERK pathway.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Leptin Signaling

Identifier	Residue	Organism
SIGNOR-261219		Homo sapiens
pmid	sentence
31643092	WB showed that BZW2 silence significantly decreased p‐ERK protein level in Colo205 cells, whereas BZW2 overexpression upregulated p‐ERK protein expression in HCT116 cells (Figure 3a,b)

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-260763		Homo sapiens
pmid	sentence
21561061	3b Augments c-Fos Levels by Activating the ERK Pathway. \| An increase of∼2.0-fold inphospho ERK (Thr-202/Tyr-204) levels in 3b-expressing Huh7cells as compared to GFP-transfected control cells (Figure 4a)was observed. This increase in phospho ERK levels was also

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism	Cell Line
SIGNOR-256093		Homo sapiens	Eosinophil
pmid	sentence
10706854	Activation of ERK2 and p38 by eotaxin is mediated through CCR3.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270138		Homo sapiens	HeLa Cell
pmid	sentence
18211802	Activates rhoa and as a result regulates actin assembly.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270204		Homo sapiens
pmid	sentence
9155017	Erk and p38 phosphorylate mnk1 and mnk2, which stimulates their in vitro kinase activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-254947		Homo sapiens	Mast Cell
pmid	sentence
15526160	A number of studies have demonstrated the ability of SCF to activate the Ras-Erk pathway. The adapter protein Grb2 can directly associate with phosphorylated Y703 and Y936 in c-Kit

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, KIT in AML, Malignant Melanoma

Identifier	Residue	Organism
SIGNOR-270131		Homo sapiens
pmid	sentence
18694962	Serum induces rhoa-dependent translocation of mkl1 from the cytoplasm to the nucleus and also causes a rapid increase in mkl1 phosphorylation. Serum-induced phosphorylation of the serum response factor coactivator mkl1 by the extracellular signal-regulated kinase 1/2 pathway inhibits its nuclear localization.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-235322		Mus musculus	3T3-L1 Cell
pmid	sentence
12270934	We demonstrate that exposure of post-confluent 3T3-L1 preadipocytes to insulin, isobutylmethylxanthine (MIX), dexamethasone (DEX), and fetal bovine serum induces a rapid but transient activation of MEK1 as indicated by extensive phosphorylation of ERK1 and ERK2 during the initial 2 h of adipogenesis. We further show that activation of MEK1 significantly enhances the transactivation of the C/EBPalpha minimal promoter during the early phase of the differentiation process.

Publications:

1

Organism:

Mus Musculus

Pathways:

Adipogenesis, Acute Myeloid Leukemia, FLT3 in AML, AML_TRIPLETS, FLT3-ITD in AML, Triple mutant AML, NPM1_new

Identifier	Residue	Organism	Cell Line
SIGNOR-253214		Homo sapiens	Lung Cancer Cell Line
pmid	sentence
12509763	Substrates for ERK1/2 include nuclear proteins such as C-JUN, this leads to activation of the AP-1 transcription factor, which is made up of FOS-JUN heterodimers.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, EGFR Signaling, Glioblastoma Multiforme, Insulin Signaling, Luminal Breast Cancer, WNT/FLT3

Identifier	Residue	Organism	Cell Line
SIGNOR-255580		Homo sapiens	Monocyte
pmid	sentence
11602185	The GM-CSF promoted cell survival and proliferation correlated with MEK-1 dependent ERK1/2, Elk-1 and CREB phosphorylation and Egr-1, c-Fos expression as well as with increased STAT-5, AP-1, c-Myb and NF-kappaB DNA-binding.

Identifier	Residue	Organism
SIGNOR-256216		Homo sapiens
pmid	sentence
20219869	ERK1/2 activation is a component of the pathway through which many mitogenic growth factors can stimulate cell proliferation

Identifier	Residue	Organism
SIGNOR-254374		Homo sapiens
pmid	sentence
24743741	Activation of PDGFRα stimulates proliferation of PDGFRα(+) cells through PI3K-Akt and MEK2-MAPK signaling pathways, and aberrant accumulation of PDGFRα(+) cells was conspicuous in muscles of patients with both genetic and non-genetic muscle diseases.

Identifier	Residue	Organism
SIGNOR-255120		Mus musculus
pmid	sentence
20219869	Furthermore, stimulation of myoblasts with CCL2, CCL3, or CCL4 was sufficient to induce phosphorylation and activation of ERK1/2. This outcome may be functionally important because ERK1/2 activation is a component of the pathway through which many mitogenic growth factors can stimulate cell proliferation.

Identifier	Residue	Organism
SIGNOR-254354		Homo sapiens
pmid	sentence
19819937	In addition to the JAK2–STAT5 pathway, the Ras GTPase–extracellular signal-regulated kinase (Ras–ERK) pathway has also been implicated in signaling of IL-5 and is important for IL-5-dependent cell survival, proliferation and differentiation of eosinophils.

Publications:

5

Organism:

Homo Sapiens, Mus Musculus

Tissue:

Skeletal Muscle

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, AMPK Signaling, B-cell activation, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD in AML, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Integrin Signaling, Luminal Breast Cancer, Leptin Signaling, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Thyroid cancer, VEGF Signaling, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-269924		Homo sapiens
pmid	sentence
21908610	Here we demonstrate that inactivation of both erk1/2 and p38_ by dusp9/mkp-4 is mediated by a conserved arginine-rich kinase interaction motif located within the amino-terminal non-catalytic domain of the protein.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-254357		Homo sapiens
pmid	sentence
11591790	We and others have recently found that eotaxin activates extracellular signal-regulated kinase (ERK)-1/2 and p38 mitogen-activated protein (MAP) kinases in eosinophils, and that these kinases are indispensable for eosinophil chemotaxis and degranulation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270168		Homo sapiens	T-lymphocyte
pmid	sentence
14768064	The precursor form of the cytokine il-16 (proil-16) was shown to be phosphorylated on ser144 in antigen receptor-, sdf1alpha- and il-2-activated t cells. Genetic and pharmacological-inhibitor experiments showed that the phosphorylation of proil-16 is dependent on activation of the kinases erk1/2. Il-16 is secreted by mitogen-activated t cells, and the biochemical link between proil-16 and erk1/2, revealed by studies with pap-1, prompted analysis of the role of map kinases in this response.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269925		Homo sapiens
pmid	sentence
11702783	Here, we report that pea-15, a protein variably expressed in multiple cell types, blocks erk-dependent transcription and proliferation by binding erks and preventing their localization in the nucleus._ Pea-15 can redirect the biological outcome of map kinase signaling by regulating the subcellular localization of erk map kinase.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-272609		Homo sapiens	HEK-293 Cell
pmid	sentence
12049732	ERK1/2 MAP kinases are important regulators in cellular signaling, whose activity is normally reversibly regulated by threonine-tyrosine phosphorylation. In contrast, we have found that stress-induced ERK1/2 activity is downregulated by ubiquitin/proteasome-mediated degradation of ERK1/2. The PHD domain of MEKK1, a RING finger-like structure, exhibited E3 ubiquitin ligase activity toward ERK2 in vitro and in vivo. Therefore, MEKK1 functions not only as an upstream activator of the ERK and JNK through its kinase domain, but also as an E3 ligase through its PHD domain, providing a negative regulatory mechanism for decreasing ERK1/2 activity.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, EGFR Signaling, SARS-CoV MAPK PERTURBATION, Toll like receptors

Identifier	Residue	Organism
SIGNOR-260656		Homo sapiens
pmid	sentence
19151752	One of the major molecular changes by NEU1 was decreased sialylation of integrin beta4, assessed by PNA- and MAL-II-lectin blotting of immunoprecipitates with anti-integrin beta4 antibody. The desialylation was accompanied by decreased phosphorylation of the integrin followed by attenuation of focal adhesion kinase and Erk1/2 pathway.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270143		Homo sapiens
pmid	sentence
12809513	We concluded that serine 142 of the tr dbd is the likely site of phosphorylation by t(4)-activated mapk and that the docking site on tr for activated mapk includes residues 128-133 (kgffrr), a basic amino acid-enriched motif novel for mapk substrates. Tr mutations in the proposed mapk docking domain and at residue 142 modulated t(4)-conditioned shedding of co-repressor and recruitment of co-activator proteins by the receptor, and they altered transcriptional activity of tr in a thyroid hormone response element-luciferase reporter assay.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270146		Homo sapiens
pmid	sentence
19282669	Phosphorylation of foxo3a by erk1/2 at residues ser 294, ser 344 and ser 425 increases foxo3amdm2 interaction and enhances foxo3a degradation via an mdm2-dependent ubiquitin-proteasome pathway

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, FLT3-ITD in AML, FLT3-ITD signaling, NPM1_new, PI3K/AKT Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-270153		Homo sapiens	Leukemia Cell
pmid	sentence
15093545	Phosphorylation of pml by mitogen-activated protein kinases plays a key role in arsenic trioxide-mediated apoptosis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-258992		Mus musculus
pmid	sentence
11730323	Raf proteins have been shown to phosphorylate and activate MAPKKs (MAP kinase kinases) called MEKs (MAPK or ERK kinases) which in turn phosphorylate and activate MAPKs (MAP kinases) called ERKs

Identifier	Residue	Organism	Cell Line
SIGNOR-235352		Mus musculus	3T3-L1 Cell
pmid	sentence
12270934	MEK1 as indicated by extensive phosphorylation of ERK1 and ERK2 during the initial 2 h of adipogenesis.

Publications:

2

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-270206		Homo sapiens
pmid	sentence
14967450	Erk phosphorylates multiple cytoplasmatic and cytoskeletal proteins, including mapk-activated protein kinases and the ribosomal p70-s6 kinase

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-270147
pmid	sentence
11493009	Specifically, the complex formation between PTP-SL and ERK2 involves an unusual interaction leading to the phosphorylation of PTP-SL by ERK2 at Thr253 and the inactivating dephosphorylation of ERK2 by PTP-SL.

Publications:

1

Identifier	Residue	Organism
SIGNOR-269933		Rattus norvegicus
pmid	sentence
7535768	Dephosphorylation and Inactivation of ERKs\|ERK1 phosphorylated on either threonine (ERK1Y204F) or tyrosine alone (ERK1T202A) was utilized as a substrate for HVH2. Threonine 202 and tyrosine 204 in ERK1 (53) correspond to threonine 183 and tyrosine 185 in ERK2 which are the activation-phosphorylation sites by MEK(14, 15, 16). ERK1, a kinase-deficient mutant, was phosphorylated on both threonine and tyrosine by MEK2 (Fig. 3B). ERK1T202A, having threonine 202 substituted by an alanine, was phosphorylated only on tyrosine while ERK1Y204F, having tyrosine 204 substituted by a phenylalanine, was phosphorylated only on threonine (Fig. 3B). GST-HVH2 dephosphorylated all three ERK1 mutants (Fig. 3A), suggesting that double phosphorylations of adjacent threonine and tyrosine were not a prerequisite for HVH2 recognition. However, HVH2 dephosphorylated ERK1* and ERK1T202A more efficiently than ERK1Y204F (Fig. 3A), indicating that HVH2 preferred phosphotyrosine over phosphothreonine. Interestingly, MEK also phosphorylated tyrosine residues more efficiently than threonine residues of ERK

Publications:

1

Organism:

Rattus Norvegicus

Identifier	Residue	Organism
SIGNOR-270165		Homo sapiens
pmid	sentence
17685427	Here, we show that sp3, which, as sp1, belongs to the gc-rich binding transcription factor family, is also phosphorylated by erk in vitro on serine 73.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269926		Homo sapiens
pmid	sentence
12840032	P-erk1/2 proteins were efficiently dephosphorylated in vitro by protein phosphatases 1 and 2a (pp1/2a) and mapk phosphatase 3 (mkp3).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270140		Homo sapiens	T-lymphocyte, Lymphoma Cell
pmid	sentence
9649500	Here we show that antigen receptor activation leads to bcl-6 phosphorylation by mitogen-activated protein kinase (mapk). Phosphorylation, in turn, targets bcl-6 for rapid degradation by the ubiquitin/proteasome pathway.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-261521		Mus musculus
pmid	sentence
14981546	These data confirm previous findings that FLT3 receptors with ITD mutations efficiently trigger the activation of ERK, STAT5 and Akt in the absence of FL stimulation.

Identifier	Residue	Organism
SIGNOR-260132		Homo sapiens
pmid	sentence
30552988	Oncogenic, constitutively active mutants of FLT3 are known to be expressed in acute myeloid leukemia and to correlate with poor prognosis. Activation of the receptor mediates cell survival, cell proliferation and differentiation of cells. Several of the signal transduction pathways downstream of FLT3 have been shown to include various members of the SRC family of kinases (SFKs). They are involved in regulating the activity of RAS/ERK pathways through the scaffolding protein GAB2 and the adaptor protein SHC.

Publications:

2

Organism:

Mus Musculus, Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, AML_TRIPLETS, FLT3-ITD in AML, FLT3-ITD signaling, Triple mutant AML, NPM1_new, WNT/FLT3

Identifier	Residue	Organism	Cell Line
SIGNOR-256080		Mus musculus	Bone Marrow-derived Macrophage
pmid	sentence
26208884	The mitogen activated protein kinases ERK1/2 play an important role in response to toll like receptor (TLR) activation and cytokine production, including IL-10 and IL-12.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-255117		Mus musculus
pmid	sentence
20219869	The investigators showed that myoblasts constitutively express receptors for CCL2 (CCR2), CCL3 (CCR1 and CCR5), and CCL4 (CCR5), and that stimulation with either CCL2 or CCL4 was sufficient to promote myoblast proliferation. Furthermore, stimulation of myoblasts with CCL2, CCL3, or CCL4 was sufficient to induce phosphorylation and activation of ERK1/2.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism	Cell Line
SIGNOR-270187		Homo sapiens	Neutrophil
pmid	sentence
16778989	Inhibitors of the erk1/2 pathway abrogated gm-csf-induced phosphorylation of ser345, while p38 mapk inhibitor abrogated tnf-alpha-induced phosphorylation of ser345.These results show that the ala-mutated p47phox acts as a dominant-negative inhibitor of endogenous p47phox and clearly indicate that phosphorylation of ser345 is required for the priming of nadph oxidase activity in neutrophil-like cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270198		Homo sapiens
pmid	sentence
14967450	Erk phosphorylates multiple cytoplasmatic and cytoskeletal proteins, including mapk-activated protein kinases and the ribosomal p70-s6 kinase

Publications:

1

Organism:

Homo Sapiens

Tissue:

Carcinoma Cell

Pathways:

FLT3-ITD signaling, Insulin Signaling, MTOR Signaling, Nucleotide Biosynthesis

Identifier	Residue	Organism
SIGNOR-255573		Homo sapiens
pmid	sentence
24890514	The Erk1/2 pathway has a central role in CSF-1R-regulated myeloid differentiation. CSF-1 induces early (peaking at ‚àº5 min) and persistent (starting at 1 h) waves of MEK/Erk1/2 phosphorylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270171		in vitro
pmid	sentence
11805112	Using a number of different approaches it was demonstrated that the protein kinase acting on betaThr-613 and gammaThr-623 is the extracellular regulated kinase (ERK). It is suggested that an ERK-mediated phosphorylation of betaThr-613 and gammaThr-623 down-regulates the channel by facilitating its interaction with Nedd4.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-270176		Homo sapiens
pmid	sentence
21385839	Phosphorylation of kinesin light chain 1 at serine 460 modulates binding and trafficking of calsyntenin-1mutation of klc1ser460 to an alanine residue, to preclude phosphorylation, increased the binding of calsyntenin-1, whereas mutation to an aspartate residueklc1ser460 is a predicted mitogen-activated protein kinase (mapk) target site, and we show that extracellular-signal-regulated kinase (erk) phosphorylates this residue in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270182		Homo sapiens	HEK-293 Cell
pmid	sentence
9731215	Stress-induced stathmin phosphorylation is not de- pendent on ERK. Stathmin is also known to be phos- phorylated by ERK on Ser-25 and Ser-38 (17). Thus, it is possible that ERK phosphorylates stathmin in 293 cells\|In subsequent reports (28, 29) it was shown that phosphorylation of stathmin blocks its ability to destabilize MTs.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-255119		Mus musculus
pmid	sentence
20219869	The investigators showed that myoblasts constitutively express receptors for CCL2 (CCR2), CCL3 (CCR1 and CCR5), and CCL4 (CCR5), and that stimulation with either CCL2 or CCL4 was sufficient to promote myoblast proliferation. Furthermore, stimulation of myoblasts with CCL2, CCL3, or CCL4 was sufficient to induce phosphorylation and activation of ERK1/2.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-269923		Homo sapiens
pmid	sentence
12840032	P-erk1/2 proteins were efficiently dephosphorylated in vitro by protein phosphatases 1 and 2a (pp1/2a) and mapk phosphatase 3 (mkp3). the dual specificity phosphatases that specifically dephosphorylate and inactivate the p-erk1/2 are called mapk phosphatases

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-261930		Homo sapiens
pmid	sentence
28137827	Binding of S100A9 to TLR4 stimulates the phosphorylation of JNK, ERK1/2, and p38 MAPK, which leads to the activation of c-Jun, CREB, and NF-κB. Activation of neutrophils by S100A9 also proceeds via p38 MAPK, JNK, and ERK1/2 phosphorylation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Organism
SIGNOR-244750		Homo sapiens
pmid	sentence
20457810	Soluble pref-1 inhibits adipocyte differentiation through the activation of extracellular signal-regulated kinase/mitogen-activated protein kinase (erk/mapk) and the subsequent upregulation of sox9 expression.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255579		Homo sapiens	Monocyte
pmid	sentence
11602185	The GM-CSF promoted cell survival and proliferation correlated with MEK-1 dependent ERK1/2, Elk-1 and CREB phosphorylation and Egr-1, c-Fos expression as well as with increased STAT-5, AP-1, c-Myb and NF-kappaB DNA-binding.

Identifier	Residue	Organism	Cell Line
SIGNOR-254948		Homo sapiens	Mast Cell
pmid	sentence
15526160	Numerous studies have implicated the critical importance of the Ras/Erk pathway in cell division and survival

Publications:

2

Organism:

Homo Sapiens

Tissue:

Skeletal Muscle

Pathways:

Colorectal Carcinoma, ErbB receptors in cancer, Glioblastoma Multiforme, Hepatocellular Tumor, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer

Identifier	Residue	Organism
SIGNOR-270203		Homo sapiens
pmid	sentence
20230789	Accumulating evidence indicates that protein phosphorylation regulates nox activity. In this report, we show that serine282 residue of nox activator 1 (noxa1) is phosphorylated by erk in response to egf resulting in desensitization of nox1 activity

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270202		in vitro
pmid	sentence
16226275	First, Erk phosphorylates HePTP at residues Thr45 and Ser72. Second, HePTP dephosphorylates Erk at PTyr185.\|

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-270167		Homo sapiens
pmid	sentence
7901013	In this paper we have studied the phosphorylation and activation of alternatively spliced forms of human th by mapkap kinase-1 , mapkap kinase-2, map kinase, and cam kinase-11

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244640		Homo sapiens
pmid	sentence
9013873	Vav may link gp130 activation to downstream mapk activation in hematopoietic cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270144		Homo sapiens
pmid	sentence
8939914	Several lines of investigation have suggested that rsk is phosphorylated and activated by erk1/2 mapk isoforms

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244761		Homo sapiens
pmid	sentence
15851026	Here, we show that erk may play a critical role in tsc progression through posttranslational inactivation of tsc2. Erk-dependent phosphorylation leads to tsc1-tsc2 dissociation and markedly impairs tsc2 ability to inhibit mtor signalin.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Insulin Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-244665		Homo sapiens	Macrophage
pmid	sentence
11842088	In addition, immunoblot and immunostaining analysis revealed that phosphorylation of erk was increased by treatment with sb203580;whereas pd98059 increased the phosphorylation of p38, which implies a seesaw-like balance between erk and p38 phosphorylation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling, Toll like receptors

Identifier	Residue	Organism
SIGNOR-270174		Homo sapiens
pmid	sentence
10828059	These straddle the target residue, ser(579), for erk2 phosphorylation of pde4d3. Mutation of either or both of these docking sites prevented erk2 from being co-immunoprecipitated with pde4d3, ablated the ability of epidermal growth factor to inhibit pde4d3 through erk2 action in transfected cos cells, and attenuated the ability of erk2 to phosphorylate pde4d3 in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270166		Homo sapiens
pmid	sentence
14697653	Thus, fe65 has at least two apparently disparate functions and may also be involved in the pathogenesis of alzheimer's disease. The mechanisms by which fe65 trafficking and metabolism are regulated to fulfil these different roles are unclear. Our findings reported here, which demonstrate that fe65 is a phosphoprotein that is targeted by erk1/2 and which identify four in vivo phosphorylation sites, provide one possible mechanism whereby functional diversity might be achieved.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-233520		Homo sapiens
pmid	sentence
23616010	Erk also undergoes rapid translocation into the nucleus, where it phosphorylates and activates a variety of transcription factor targets, including sp1, e2f, elk-1, and ap1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, Glioblastoma Multiforme, IL6 Signaling, Integrin Signaling, Noonan syndrome

Identifier	Residue	Organism
SIGNOR-270161		Homo sapiens
pmid	sentence
21419341	We show that erk colocalizes with the wrc at lamellipodial leading edges and directly phosphorylates two wrc components: wave2 and abi1.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-269920		Mus musculus	NIH-3T3 Cell
pmid	sentence
11742987	Both induction of MKP-1 expression and inhibition of its degradation are necessary for glucocorticoid-mediated inhibition of Erk-1/2 activation.

Publications:

1

Organism:

Mus Musculus

Pathways:

Adipogenesis

Identifier	Residue	Organism
SIGNOR-255572		Homo sapiens
pmid	sentence
24890514	The Erk1/2 pathway has a central role in CSF-1R-regulated myeloid differentiation. CSF-1 induces early (peaking at ‚àº5 min) and persistent (starting at 1 h) waves of MEK/Erk1/2 phosphorylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-263499		Homo sapiens
pmid	sentence
11085989	We show here that leptin can activate ERK signaling in thehypothalamus and that this stimulation is likely to occur viatwo pathways, both involving SHP-2.We have shown above that SHP-2 is a positive mediator of ERK activation by ObRb and that this requires both the phosphatase activity and tyrosine phosphorylation of SHP-2. Furthermore,Tyr-985 is required for maximal ERK phosphorylation.

Identifier	Residue	Organism
SIGNOR-263500		Homo sapiens
pmid	sentence
11085989	We show here that leptin can activate ERK signaling in thehypothalamus and that this stimulation is likely to occur viatwo pathways, both involving SHP-2.We have shown above that SHP-2 is a positive mediator of ERK activation by ObRb and that this requires both the phosphatase activity and tyrosine phosphorylation of SHP-2. Furthermore,Tyr-985 is required for maximal ERK phosphorylation.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, KIT in AML, AML_TRIPLETS, EGFR Signaling, FLT3-ITD signaling, Leptin Signaling, NPM1_new, Noonan syndrome

Identifier	Residue	Organism
SIGNOR-270170		in vitro
pmid	sentence
9525907	In vitro, purified mitogen-activated protein (MAP) kinase catalyzed the phosphorylation of Graf on serine 510, suggesting that Graf phosphorylation may be mediated through MAP kinase signaling.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-262519		Mus musculus	MEF Cell
pmid	sentence
28646232	We demonstrate that insulin-mediated activation of ERK1/2 results in phosphorylation of GSK3β at S9 independently of Akt/mTORC1 activity in Tsc2 null mouse embryonic fibroblasts. In addition, we show that inhibition of ERK1/2 rescues GSK3β activity and restores protein synthesis in Tsc2 −/− MEFs to normal levels

Publications:

1

Organism:

Mus Musculus

Pathways:

Colorectal Carcinoma, Hepatocellular Tumor

Identifier	Residue	Organism
SIGNOR-270175		Homo sapiens
pmid	sentence
19282669	Phosphorylation of foxo3a by erk1/2 at residues ser 294, ser 344 and ser 425 increases foxo3amdm2 interaction and enhances foxo3a degradation via an mdm2-dependent ubiquitin-proteasome pathway

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3 in AML, AMPK Signaling, Insulin Signaling, Inhibition of Apoptosis, Integrin Signaling, Thyroid cancer

Identifier	Residue	Organism
SIGNOR-270193		in vitro
pmid	sentence
15133517	To identify the phosphorylated residue, we introduced a serine-to-alanine substitution at residues 294 and 326 and a threonine-to-alanine substitution at residue 331 in Irx2(291‚Äì356). Erk1 phosphorylated S294A and T331A, but not S326A (Fig. 4b), indicating that Ser326 is the bona fide MAP kinase target.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-256078		Mus musculus	B-lymphocyte, Macrophage
pmid	sentence
16484370	Mitogen-activated protein 3 kinase Tpl2, levels of which are markedly reduced in nfkb1(-/-) cells, is required for extracellular signal-regulated kinase (ERK) activation in bone marrow-derived macrophages and B cells stimulated with diverse TLR ligands

Publications:

1

Organism:

Mus Musculus

Pathways:

Toll like receptors

Identifier	Residue	Organism	Cell Line
SIGNOR-259174		Mus musculus	NIH-3T3 Cell
pmid	sentence
21415216	We also found that phosphorylation of both the mitogen-activated proteinkinase (MAPK) ERK and STAT3 was markedly increased inthe cells expressing either variant of EML4-ALK[.]. Oncogenic EML4-ALK tyrosine kinase activates ERKand STAT3 signaling pathways

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism	Cell Line
SIGNOR-263067		Homo sapiens	HEK-293 Cell
pmid	sentence
20622900	These two KIM sites are found at N- and C-terminal locations on hScrib, and both are essential for directing the interaction between ERK and hScrib, but with the C-terminal site having the strongest affinity for ERK. One of the most likely consequences of this interaction is to inhibit ERK translocation to the nucleus.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-260082		Homo sapiens
pmid	sentence
21900390	RAF, a cytoplasmic serine-threonine protein kinase, is a member of the RAS-RAF-MEK-ERK cell-signaling pathway [also known as the MAP kinase (MAPK) pathway], and it plays an essential role in mediating cellular differentiation, proliferation, senescence, and survival in response to extracellular cues. Raf phosphorylates and activates MAP-ERK kinase (MEK), which phosphorylates and activates extracellular signal-regulated kinase (ERK).

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-270177		Homo sapiens	HeLa Cell
pmid	sentence
8618896	Phosphorylation at Ser-59 (or alternatively, its mutation to Glu) reverses the inhibition and allows interaction of the p56lck SH2 domain with p62.\|phosphotyrosine-independent binding of p62 to the p56lck SH2 domain appears to provide an alternative pathway for p56lck signaling that is regulated by Ser-59 phosphorylation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

T cell activation

Identifier	Residue	Organism
SIGNOR-254687		Homo sapiens
pmid	sentence
21364186	Lowering the extent of costimulation of P2X in T cells diminishes the extent of ERK phosphorylation without affecting TCR-mediated nuclear translocation of NFAT (10). In Tregs, this mechanism would favor the stability of their transcriptional program through the stabilization of nuclear complexes of NFAT and Foxp3 (47).

Identifier	Residue	Organism
SIGNOR-254686		Homo sapiens
pmid	sentence
23620016	In the current study, addition of ERK inhibitors suppressed IL-6-induced RORgammat expression and promoted TGF-beta-induced Foxp3 expression.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270156		Homo sapiens
pmid	sentence
14662762	Erk1/2 are major ser-5 kinases after h2o2 treatment. These results suggest that subsequent to h2o2 treatment, the ser-5-phosphorylated form, but not the ser-2-phosphorylated form or the unphosphorylated form, is targeted for rapid proteasomal degradation through its ubiquitination.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-270135
pmid	sentence
16554440	Also, several probable in vivo K8 kinases have been identified including Erk1/2 for K8 Ser431 (Ku and Omary, 1997), and p38 and Jun kinases for K8 Ser73 (Ku et al., 2002a; He et al., 2002).

Publications:

1

Identifier	Residue	Organism
SIGNOR-255118		Mus musculus
pmid	sentence
20219869	The investigators showed that myoblasts constitutively express receptors for CCL2 (CCR2), CCL3 (CCR1 and CCR5), and CCL4 (CCR5), and that stimulation with either CCL2 or CCL4 was sufficient to promote myoblast proliferation. Furthermore, stimulation of myoblasts with CCL2, CCL3, or CCL4 was sufficient to induce phosphorylation and activation of ERK1/2.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism	Cell Line
SIGNOR-270149		Mus musculus	C2C12 Cell
pmid	sentence
12063245	Consensus phosphorylation sites for p42/44 MAPK and GSK-3 are present in the SP repeat of MCIP1 at serine 112 and serine 108, respectively \|Several endogenous proteins are capable of inhibiting the catalytic activity of calcineurin. Modulatory calcineurin interacting protein 1 (MCIP1) is unique among these proteins on the basis of its pattern of expression and its function in a negative feedback loop to regulate calcineurin activity. Here we show that MCIP1 can be phosphorylated by MAPK and glycogen synthase kinase-3 and that phosphorylated MCIP1 is a substrate for calcineurin.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism	Cell Line
SIGNOR-235334		Mus musculus	3T3-L1 Cell
pmid	sentence
12270934	Our results suggest that activation of the MEK/ERK signaling pathway during the initial 12 h of adipogenesis enhances the activity of factors that regulate both C/EBPalpha and PPARgamma expression.

Publications:

1

Organism:

Mus Musculus

Pathways:

Adipogenesis, Leptin Signaling, MTOR Signaling, Rett syndrome, Thyroid cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-270194		Homo sapiens	Prostate Gland Cancer Cell
pmid	sentence
12163482	Mapk also directly phosphorylates src-1 at thr1179 and ser1185. Phosphorylation of src-1 by mitogen-activated protein kinase (mapk) is required for optimal progesterone receptor-dependent transcription and for functional cooperation with camp response element-binding protein-binding protein

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia

Identifier	Residue	Organism
SIGNOR-269919		Homo sapiens
pmid	sentence
12771128	A dominant-negative mutant of high cell densityenhanced ptp 1 (dep-1)//cd148 as well as reduction of its expression by rna interference partially restore vegfr-2 phosphorylation and map kinase activation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3-ITD in AML

Identifier	Residue	Organism
SIGNOR-270183		Homo sapiens
pmid	sentence
22327296	Menin binds the jun family transcription factor jund and inhibits its transcriptional activity. The menin-jund interaction blocks jun n-terminal kinase (jnk)-mediated jund phosphorylation and suppresses jund-induced transcription. We found a role for phosphorylation of the ser100 residue of jund;jund phosphorylation were prevented by inhibitors of calcium, calmodulin, or erk1/2 kinase.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270186		Homo sapiens
pmid	sentence
14993270	Activated erk can phosphorylate t292 in the prs, and this blocks the ability of pak to phosphorylate s298 and of rac-pak signaling to enhance mek1-erk complex formation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, T cell activation, Toll like receptors

Identifier	Residue	Organism
SIGNOR-270190		Homo sapiens
pmid	sentence
10347142	Erk1 and erk2 phosphorylate beta-arrestin1 at ser-412 in vitro. . in the resting state, cytosolic arrestin1 proteins are constitutively phosphorylated by extracellular signal-regulated kinase (erk) at ser412, located within their distal c terminus. erk-phosphorylated arrestin1 is unable to associate with clathrin cages, whereas this constraint is removed upon its dephosphorylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270197		Homo sapiens
pmid	sentence
15262992	Thus, we propose that mapk phosphorylation of amphiphysin1 controls ngf receptor/trka-mediated endocytosis by terminating the amphiphysin1-ap-2 interaction.Our results indicate that phosphorylation of amphiphysin 1 at ser-285 and/or ser-293 affects the function of amphiphysin1.Mapk phosphorylation of ser-285 and ser-293 could modulate the interaction between prd and ap-2, resulting in the dissociation of amphiphysin1 from ap-2.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Organism	Cell Line
SIGNOR-269928		Chlorocebus aethiops	COS Cell
pmid	sentence
10224087	Extracellular regulated kinases (ERK) 1 and ERK2 are authentic substrates for the dual-specificity protein-tyrosine phosphatase VHR. A novel role in down-regulating the ERK pathway.\|Catalysis by VHR requires the native structure of ERK and is specific for tyrosine 185 of ERK2

Publications:

1

Organism:

Chlorocebus Aethiops

Identifier	Residue	Organism
SIGNOR-270195		Homo sapiens
pmid	sentence
16401070	Phosphorylation decreased the ability of mbp to polymerize actin and to bundle actin filaments but had no effect on the dissociation constant of the mbp-actin complex or on the ability of ca2+-calmodulin to dissociate the complex. The most significant effect of phosphorylation on the mbp-actin complex was a dramatic reduction in its ability to bind to negatively charged lipid bilayers. The identification of myelin basic protein (phosphorylation at -pro-arg-thr-pro-) as a substrate for the erk kinases (fig. 1) demonstrates that there are other determinants important for substrate recognition than those present in the originally identified consensus sequence.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Organism
SIGNOR-270189		Homo sapiens
pmid	sentence
16286470	The dual-specificity mapk phosphatase mkp-1/cl100/dusp1 is an inducible nuclear protein controlled by p44/42 mapk (erk1/2) in a negative feedback mechanism to inhibit kinase activity. Here, we report on the molecular basis for a novel positive feedback mechanism to sustain erk activation by triggering mkp-1 proteolysis. Active erk2 docking to the def motif (fxfp, residues 339-342) of n-terminally truncated mkp-1 in vitro initiated phosphorylation at the ser(296)/ser(323) domain

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270160		Homo sapiens
pmid	sentence
15657420	The formation of rsk-nfatc4-dna transcription complex is also apparent upon adipogenesis. Bound rsk phosphorylates ser(676) and potentiates nfatc4 dna binding by escalating nfat-dna association. Ser(676) is also targeted by the erk map kinase, which interacts with nfat at a distinct region than rsk. Thus, integration of the erk/rsk signaling pathway provides a mechanism to modulate nfatc4 transcription activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270157		Homo sapiens	Breast Cancer Cell
pmid	sentence
10655479	Specifically, down-regulation of mature prs occurs by a mechanism in which ligand binding activates pr phosphorylation by mapks at a unique serine residue, which then targets the receptors for degradation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-233523		Homo sapiens
pmid	sentence
23616010	Erk also undergoes rapid translocation into the nucleus, where it phosphorylates and activates a variety of transcription factor targets, including sp1, e2f, elk-1, and ap1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML

Identifier	Residue	Organism	Cell Line
SIGNOR-270164		Homo sapiens	Neuron
pmid	sentence
20444238	Cortactin is regulated by multiple phosphorylation events, including phosphorylation of s405 and s418 by extracellular regulated kinases (erk)1/2. Erk1/2 phosphorylation of cortactin has emerged as an important positive regulatory modification, enabling cortactin to bind and activate the arp2/3 regulator neuronal wiskott-aldrich syndrome protein (n-wasp), promoting actin polymerization and enhancing tumor cell movement.

Publications:

1

Organism:

Homo Sapiens

Pathways:

T cell activation

Identifier	Residue	Organism	Cell Line
SIGNOR-269921		Homo sapiens	T-lymphocyte
pmid	sentence
17998336	The sh3 domain of lck modulates t-cell receptor-dependent activation of extracellular signal-regulated kinase through activation of raf-1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

T cell activation

Identifier	Residue	Organism
SIGNOR-269929		Homo sapiens
pmid	sentence
20974802	We show that several proline-directed mitogen-activated protein kinases (mapks), such as p38, erk1/2, and jnk1 are sufficient and required for the phosphorylation of ppps/tp motifs of lrp6. External stimuli, which control the activity of mapks, such as phorbol esters and fibroblast growth factor 2 (fgf2) control the choice of the lrp6-ppps/tp kinase and regulate the amplitude of lrp6 phosphorylation and wnt/beta-catenin-dependent transcription.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269932		Homo sapiens
pmid	sentence
10224087	Extracellular regulated kinases (erk) 1 and erk2 are authentic substrates for the dual-specificity protein-tyrosine phosphatase vhr. A novel role in down-regulating the erk pathway

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270181		Homo sapiens
pmid	sentence
11741541	Erk1/2 was found to phosphorylate the architectural transcription factor ubf at amino acids 117 and 201 within hmg boxes 1 and 2, preventing their interaction with dna

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia

Identifier	Residue	Organism
SIGNOR-244643		Homo sapiens
pmid	sentence
16153436	We hypothesized that ret could directly phosphorylate fak and erk. erk 2 could be phosphorylated at y187 (y204 in erk1).

Publications:

1

Organism:

Homo Sapiens

Pathways:

Thyroid cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-244862		Chlorocebus aethiops	COS Cell
pmid	sentence
14993270	We propose that activation of erk during adhesion creates a feedback system in which erk phosphorylates mek1 on t292, and this in turn blocks additional s298 phosphorylation in response to integrin signaling.

Identifier	Residue	Organism	Cell Line
SIGNOR-244858		Homo sapiens	HEK-293 Cell
pmid	sentence
10567369	An ERK2-binding site at the N terminus of MEK1 was reported to mediate their stable association. We examined the importance of this binding site in the feedback phosphorylation of mek1 on thr(292) and thr(386) by erk2

Publications:

2

Organism:

Chlorocebus Aethiops, Homo Sapiens

Pathways:

Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, B-cell activation, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Inhibition of Apoptosis, Integrin Signaling, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Oxytocin signaling, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Thyroid cancer, T cell activation, Toll like receptors, VEGF Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-270207		Mus musculus	NIH-3T3 Cell
pmid	sentence
11581251	Thus, activation of the ERK pathway appears to be able to regulate adipocyte lipolysis by phosphorylating HSL on Ser(600) and increasing the activity of HSL.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-270155		Homo sapiens
pmid	sentence
10906323	Pttg is phosphorylated in vitro on ser(162) by map kinase and this phosphorylation site plays an essential role in pttg transactivation function.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270136		Homo sapiens
pmid	sentence
10194762	Serine 780 is the only substrate in full-length stat5a for active erk

Publications:

1

Organism:

Homo Sapiens

Tissue:

Ovary

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, B-cell activation, FLT3-ITD in AML, FLT3-ITD signaling, Leptin Signaling, Triple mutant AML

Identifier	Residue	Organism
SIGNOR-270179		Homo sapiens
pmid	sentence
14993287	Epidermal growth factor activates m-calpain (calpain ii), at least in part, by extracellular signal-regulated kinase-mediated phosphorylation.We now show that erk directly phosphorylates and activates m-calpain both in vitro and in vivo. We identified serine 50 as required for epidermal growth factor (egf)-induced calpain activation in vitro and in vivo.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270210		Homo sapiens
pmid	sentence
12050114	Tob is rapidly phosphorylated at Ser 152, Ser 154, and Ser 164 by Erk1 and Erk2 upon growth-factor stimulation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270141		Homo sapiens
pmid	sentence
14988395	Insulin-activated erk-mitogen-activated protein kinases phosphorylate sterol regulatory element-binding protein-2 at serine residues 432 and 455 in vivo.Further characterization by electrophoretic mobility shift assay and promoter reporter gene analyses revealed that phosphorylation does not influence protein/dna interaction, but enhances trans-activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270150		Homo sapiens
pmid	sentence
21071439	We found three proline-directed residues within raptor, ser(8), ser(696), and ser(863), which are directly phosphorylated by erk1/2. Expression of phosphorylation-deficient alleles of raptor revealed that phosphorylation of these sites by erk1/2 normally promotes mtorc1 activity and signaling to downstream substrates, such as 4e-bp1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

AMPK Signaling, EGFR Signaling, Glioblastoma Multiforme, Insulin Signaling, Luminal Breast Cancer, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-270208		Homo sapiens
pmid	sentence
24269383	We demonstrated that erk1/2 phosphorylate kibra at ser(548) in cells as well as in vitro.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Breast

Identifier	Residue	Organism
SIGNOR-270172		Homo sapiens
pmid	sentence
19076070	Here we report that ews and ews-fli1 become phosphorylated at thr79 in the n-terminal domain in response to mitogens or dna damage. Mitogen-induced phosphorylation of ews and ews-fli1 was weak and catalysed by erk1 (extracellular signal-regulated kinase 1) and erk2.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270158		Homo sapiens	Breast Cancer Cell
pmid	sentence
18676833	We then showed that erk could phosphorylate mcl-1 at two consensus residues, thr 92 and 163, which is required for the association of mcl-1 and pin1, resulting in stabilization of mcl-1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, COVID-19 Causal Network

Identifier	Residue	Organism
SIGNOR-254373		Homo sapiens
pmid	sentence
18483217	PDGF signaling has been implicated in several fibrotic conditions and is assumed to play a role in driving proliferation of cells with a myofibroblast phenotype.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network

Identifier	Residue	Organism
SIGNOR-270134		Homo sapiens
pmid	sentence
7777512	Thus, our results identify the human lifr as a substrate for mapk and suggest a mechanism of heterologous receptor regulation of lifr signaling occurring at ser-1044.

Publications:

1

Organism:

Homo Sapiens

Pathways:

IL6 Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-241977		Mus musculus	P-19 Cell
pmid	sentence
24942200	During neural fate specification, nuclear translocation of ERK1/2 is critical for its activation of Sox2 transcription. More-over, melatonin-induced Sox2 expression, through ERK1/ 2 activation, could locate between base pairs2719 and 1708 in the mouse Sox2 gene.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-270173		Homo sapiens
pmid	sentence
18245089	In this study we show that the extracellular signal-regulated kinases 1 and 2 (erk1/2) interact directly with ciita, targeting serine residues in the amino terminus of the protein, including serine 288. These data suggest a model whereby erk1/2-mediated phosphorylation of ciita down-regulates ciita activity by priming it for nuclear export, thus providing a means for cells to tightly regulate the extent of antigen presentation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270152		Homo sapiens
pmid	sentence
15486195	In vitro, bimel was phosphorylated by extracellular signal-regulated kinase on ser(69), which resides in the bimel-specific insert region. Using phosphospecific antibody against this site, we show that this residue is actually phosphorylated in cells. We also show that phosphorylation of ser(69) promotes ubiquitination of bimel. We conclude that mek inhibitors sensitize mda-mb231 and hbc4 cells to anoikis by blocking phosphorylation and hence degradation of bimel

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Inhibition of Apoptosis

Identifier	Residue	Organism
SIGNOR-258995		Mus musculus
pmid	sentence
11730323	Raf proteins have been shown to phosphorylate and activate MAPKKs (MAP kinase kinases) called MEKs (MAPK or ERK kinases) which in turn phosphorylate and activate MAPKs (MAP kinases) called ERKs

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-270133		Homo sapiens
pmid	sentence
15356145	Phosphorylation of grb2-associated binder 2 on serine 623 by erk mapk regulates its association with the phosphatase shp-2 and decreases stat5 activation.We and others have demonstrated that il-2-induced tyrosine phosphorylation of gab2 and its interaction with its sh2 domain-containing partners, shp-2, p85 pi3k, and crkl (5, 26, 27). we report that pretreatment of kit 225 cells with the mek inhibitor u0126, strongly decreased the characteristic shift of gab2 in response to il-2 and increased gab2/shp-2 association, an effect that could be ascribed to erk phosphorylation of serine 623.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244637		Homo sapiens
pmid	sentence
11971971	Mapk1 is phosphorylated by map2k1/mek1 and map2k2/mek2 on thr-185 and tyr-187 in response to external stimuli like insulin or ngf. Both phosphorylations are required for activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270188		Homo sapiens	HEK-293 Cell
pmid	sentence
25728771	When phosphorylated by ERK, MCRIP1 dissociates from CtBP, allowing CtBP to interact with ZEB1. In this manner, the CtBP co-repressor complex is recruited to, and silences, the E-cadherin promoter by inducing chromatin modifications.\| While substitution of S4 or S18 with Ala did not affect the phosphorylation of MCRIP1 by ERK, substitution of either S21 or T30 significantly reduced MCRIP1 phosphorylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270151		Homo sapiens
pmid	sentence
15788406	Oxysterols inhibit phosphatidylcholine synthesis via erk docking and phosphorylation of ctp:phosphocholine cytidylyltransferase. Mutagenesis of ser315 within cctalpha was both required and sufficient to confer significant resistance to 22-hc/9-cis-ra inhibition of ptdcho synthesis.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Lung

Identifier	Residue	Organism
SIGNOR-269930		Homo sapiens
pmid	sentence
10617468	The mitogen-activated protein (map) kinase cascade is inactivated at the level of map kinase by members of the map kinase phosphatase (mkp) family, including mkp-1.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269931		Homo sapiens
pmid	sentence
12840032	When cells are stimulated with various ligands such as growth factors, hormones, neurotransmitters, or tumor promoters, erk1/2 is activated through dualphosphorylation at the -ptepy-motif. Subsequently, p-erk1/2 translocates into the nucleus and phosphorylates elk-1, thereby acting as a transcription factor for cell proliferationthese data indicate that sa-p-erk1/2 might not only be regulated by mkp such as rvhr, but also by pp1 and ptp as well

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270180		Homo sapiens	Hep-G2 Cell
pmid	sentence
10187842	We now demonstrate that amino acids 1-92 of hPPARalpha contain an activation function (AF)-1-like domain, which is further activated by insulin through a pathway involving the mitogen-activated protein kinases p42 and p44. Further analysis of the amino-terminal region of PPARalpha revealed that the insulin-induced trans-activation occurs through the phosphorylation of two mitogen-activated protein kinase sites at positions 12 and 21, both of which are conserved across evolution.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-236767		Homo sapiens	SW-620 Cell
pmid	sentence
23616010	The results revealed that PAR2-AP and FVIIa could upregulate c-Jun expression and c-Jun phosphorylation in SW620 cells in a time-dependent manner. The effect of FVIIa was significantly blocked by anti-TF and anti-PAR2 antibodies. Protein kinase C_ (PKC_) inhibitor safingol and extracellular signal-regulated kinase 1 and 2 (ERK1/2) inhibitor U0126 abrogated the activation of c-Jun

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, EGFR Signaling, Glioblastoma Multiforme, Insulin Signaling, Luminal Breast Cancer, WNT/FLT3

Identifier	Residue	Organism
SIGNOR-270185		Homo sapiens
pmid	sentence
23024368	Phosphorylation of this site downregulates nanog, sox2, rex1 and upregulates bmp4, gata6, ddlx5.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270169		Homo sapiens
pmid	sentence
10648599	Tfii-i can be phosphorylated in vitro by erk and mutation of consensus map kinase substrate sites at serines 627 and 633 impairs the phosphorylation of tfii-i by erk and its activity on the c-fos promoter. These results suggest that erk regulates the activity of tfii-i by direct phosphorylation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270139		Mus musculus	NIH-3T3 Cell
pmid	sentence
14592976	Notch-induced degradation requires phosphorylation of E47 by p42/p44 MAP kinases. \|Wild_type E47 but not the Mm mutant reacted to the antibodies, suggesting that E47 is at least phosphorylated at the M2 site (Figure 3A)\|anti_phospho_M2 peptide (SSPSpTPVGSPQG)

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-254377		Homo sapiens
pmid	sentence
24743741	To further investigate the signaling pathway through which PDGFRαpromotes the proliferation of PDGFRα+ cells, we used inhibitors of PI3K-Akt and Ras-MAPK pathways, which are known to be downstream signaling pathways of PDGFRα. Thus, both PI3K-Akt and MEK2-MAPK pathways are necessary for PDGFRα-driven proliferation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Rhabdomyosarcoma

Identifier	Residue	Organism	Cell Line
SIGNOR-270209		Homo sapiens	Breast Cancer Cell
pmid	sentence
21502402	Phosphorylation of serine 68 of twist1 by mapks stabilizes twist1 protein and promotes breast cancer cell invasiveness. this ser 68 is phosphorylated by p38, c-jun n-terminal kinases (jnk), and extracellular signal-regulated kinases1/2 in vitro

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia

Identifier	Residue	Organism
SIGNOR-270196		Homo sapiens
pmid	sentence
16456541	Iex-1 binds to b56 subunits and perk independently, enhances b56 phosphorylation by erk at a conserved ser/pro site in this complex and triggers dissociation from the catalytic subunit.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-255033		Homo sapiens
pmid	sentence
26194464	TbRI phosphorylates not only the C-termini of R-Smads but also activates various protein kinases including mitogen-activated protein kinases (MAPKs): extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 MAPK (p38), which then phosphorylate the variable linker regions of R-Smad

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, COVID-19 Causal Network, Colorectal Carcinoma, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, Thyroid cancer

Identifier	Residue	Organism
SIGNOR-270162		Homo sapiens
pmid	sentence
10514499	Extracellular signal-regulated kinases (erks) phosphorylate the high molecular mass isoform of the actin-binding protein caldesmon (h-cad) at two sites (ser(759) and ser(789)) during smooth muscle stimulation. Nmr spectroscopy shows that the actin binding properties of the minimal inhibitory region of caldesmon, residues 750-779, alter upon map kinase phosphorylation of ser-759, a residue not involved in actin binding. This phosphorylation leads to markedly diminished actin affinity as a result of the loss of interaction at one of the two sites that bind to f-actin.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Smooth Muscle

Identifier	Residue	Organism
SIGNOR-270163		in vitro
pmid	sentence
11805112	Using a number of different approaches it was demonstrated that the protein kinase acting on betaThr-613 and gammaThr-623 is the extracellular regulated kinase (ERK). It is suggested that an ERK-mediated phosphorylation of betaThr-613 and gammaThr-623 down-regulates the channel by facilitating its interaction with Nedd4.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-270205		Homo sapiens
pmid	sentence
15632084	Phosphorylation of serines 159 and 197 by erk1/2 enhances proteasomal degradation of mkp-3

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244776		Homo sapiens
pmid	sentence
11971971	Mapk1 is phosphorylated by map2k1/mek1 and map2k2/mek2 on thr-185 and tyr-187 in response to external stimuli like insulin or ngf. Both phosphorylations are required for activity.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, B-cell activation, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Inhibition of Apoptosis, Integrin Signaling, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Oxytocin signaling, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Thyroid cancer, T cell activation, Toll like receptors, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-244576		Homo sapiens
pmid	sentence
10197981	These results suggest that oncogenic ras, acting through mek1 and erk kinases, induces the phosphorylation of smad2 and smad3

Publications:

1

Organism:

Homo Sapiens

Tissue:

Lung, Breast

Pathways:

Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Organism	Cell Line
SIGNOR-242628		Mus musculus	NIH-3T3 Cell
pmid	sentence
17673906	We report that upon TGF__ stimulation, the activated TGF__ type I receptor (T_RI) recruits and directly phosphorylates ShcA proteins on tyrosine and serine. This dual phosphorylation results from an intrinsic T_RI tyrosine kinase activity that complements its well_defined serine_threonine kinase function. TGF___induced ShcA phosphorylation induces ShcA association with Grb2 and Sos, thereby initiating the well_characterised pathway linking receptor tyrosine kinases with Erk MAP kinases.

Publications:

1

Organism:

Mus Musculus

Pathways:

Acute Myeloid Leukemia, EGFR Signaling, FLT3-ITD in AML, IL6 Signaling, Noonan syndrome, Thyroid cancer

Identifier	Residue	Organism	Cell Line
SIGNOR-275411		Homo sapiens	T-lymphocyte
pmid	sentence
22740686	MEK1/2 was phosphorylated and activated upon activation of T cells through TCR-CD3 and CD28, which resulted in phosphorylation of its downstream target ERK1/2, as determined by Western blotting analysis with an antibody specific for ERK1/2 phosphorylated at Thr202 and Tyr204, markers of activation. PD-1 substantially inhibited the activation of MEK1/2 and ERK1/2

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-260660		Homo sapiens
pmid	sentence
21084287	Here we show that NPC2 deficiency in human fibroblasts confers their activation. The activation phenomenon was not limited to fibroblasts as it was also observed in aortic smooth muscle cells upon silencing NPC2 gene by siRNA. The molecular mechanism responsible for activation of NPC2-null cells was shown to be a sustained phosphorylation of ERK 1/2 mitogen-activated protein kinase (MAPK), which fulfills both the sufficient and necessary fibroblast activation criteria. All of these findings highlight a novel mechanism where NPC2 by negatively regulating ERK 1/2 MAPK phosphorylation may efficiently suppress development of maladaptive tissue remodeling and inflammation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270184		Homo sapiens
pmid	sentence
12792650	Inhibition of caspase-9 through phosphorylation at thr 125 by erk mapk

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Inhibition of Apoptosis

Identifier	Residue	Organism
SIGNOR-254355		Homo sapiens
pmid	sentence
19819937	In addition to the JAK2–STAT5 pathway, the Ras GTPase–extracellular signal-regulated kinase (Ras–ERK) pathway has also been implicated in signaling of IL-5 and is important for IL-5-dependent cell survival, proliferation and differentiation of eosinophils.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, KIT in AML, AML_TRIPLETS, B-cell activation, FLT3-ITD in AML, Triple mutant AML, NPM1_new

Identifier	Residue	Organism	Cell Line
SIGNOR-270191		Homo sapiens	HeLa Cell
pmid	sentence
18519666	We show that at least two different nuclear protein kinases, one of them identified as p42/p44 mapk, can modify hif-1_. Analysis of in vitro phosphorylated hif-1_ by mass spectroscopy revealed residues ser-641 and ser-643 as possible mapk phosphorylation sites these data suggest that phosphorylation of ser-641/643 by mapk promotes the nuclear accumulation and transcriptional activity of hif-1_

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244497		in vitro
pmid	sentence
8929531	The rapid phosphorylation of bad following il-3 connects a proximal survival signal with the bcl-2 family, modulating this checkpoint for apoptosis.phosphorylatedBAD is bound to 14-3-3 within the cytosol, while only nonphosphorylated BAD is heterodimerized with membrane-bound BCL-XL.

Publications:

1

Organism:

In Vitro

Pathways:

Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, Inhibition of Apoptosis, Malignant Melanoma, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-269918		Homo sapiens
pmid	sentence
12840032	P-erk1/2 proteins were efficiently dephosphorylated in vitro by protein phosphatases 1 and 2a (pp1/2a) and mapk phosphatase 3 (mkp3).

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, PI3K/AKT Signaling

Identifier	Residue	Organism
SIGNOR-270178		Homo sapiens
pmid	sentence
15952796	Phosphorylation of grb10 by mitogen-activated protein kinase: identification of ser150 and ser476 of human grb10zeta as major phosphorylation sitesreplacing ser(150) and ser(476) with alanines reduced the inhibitory effect of human grb10zeta on insulin-stimulated irs1 tyrosine phosphorylation

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD signaling

Identifier	Residue	Organism
SIGNOR-270142		Homo sapiens
pmid	sentence
10197981	These results suggest that oncogenic ras, acting through mek1 and erk kinases, induces the phosphorylation of smad2 and smad3.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Lung, Breast

Pathways:

Adipogenesis, COVID-19 Causal Network, Colorectal Carcinoma, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Organism	Cell Line
SIGNOR-270148		Homo sapiens	HeLa Cell
pmid	sentence
9535909	These studies confirm that connexin-43 is a MAP kinase substrate in vivo and that phosphorylation on Ser255, Ser279, and/or Ser282 initiates the down-regulation of gap junctional communication. Studies with connexin-43 mutants suggest that MAP kinase phosphorylation at one or more of the tandem Ser279/Ser282 sites is sufficient to disrupt gap junctional intercellular communication.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-254350		Homo sapiens
pmid	sentence
21106848	Human blood eosinophils exhibit a hyperactive phenotype in response to chemotactic factors after cell priming with IL-5 family cytokines. Earlier work has identified ERK1/2 as molecular markers for IL-5 priming

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-262313		Homo sapiens	HuH-7 Cell
pmid	sentence
25487801	Inhibitors of MEK1/2 (trametinib) and/or ERK1/2 (selumetinib) had the strongest and most conserved inhibitory activities, suggesting that MEK1/2 and ERK1/2 may have unique capabilities as stand-alone or combinatorial therapies for MERS-CoV infections.

Publications:

1

Organism:

Homo Sapiens

Pathways:

SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism
SIGNOR-254983		Homo sapiens
pmid	sentence
18423386	Altogether, these data suggest that PLD acting upstream of the MAP kinases ERK1/2 may play a key role in the regulation of IL-2 production by stimulated Jurkat cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-255586		Homo sapiens	Monocyte
pmid	sentence
19436055	As a consequence of Jak2 activation and tyrosine phosphorylation of the cytoplasmic tail of beta-c, Src homology 2 and phosphotyrosine binding domain proteins are recruited to the active receptor and initiate the major tyrosine phosphorylation-dependent signaling pathways, including the Jak/signal transducer and activator of transcription, Ras/mitogen-activated protein kinase, and phosphatidylinositol 3 (PI-3) kinase pathways

Publications:

1

Organism:

Homo Sapiens

Tissue:

Skeletal Muscle

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML

Identifier	Residue	Organism
SIGNOR-270192		Homo sapiens
pmid	sentence
8381049	Activated map kinase phosphorylates cpla2 at ser-505, causing increased enzymatic activity of cpla2, which is only realized upon translocation of cpla2 to the membrane.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-270154		Homo sapiens	Breast Cancer Cell
pmid	sentence
17311928	Sphingosine kinase type 2 activation by erk-mediated phosphorylation. site-directed mutagenesis indicated that hsphk2 is phosphorylated on ser-351 and thr-578 by erk1

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-258989		Mus musculus
pmid	sentence
11730323	Raf proteins have been shown to phosphorylate and activate MAPKKs (MAP kinase kinases) called MEKs (MAPK or ERK kinases) which in turn phosphorylate and activate MAPKs (MAP kinases) called ERKs

Publications:

1

Organism:

Mus Musculus

Pathways:

Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, B-cell activation, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Inhibition of Apoptosis, Integrin Signaling, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Oxytocin signaling, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Thyroid cancer, T cell activation, Toll like receptors, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-270132		Homo sapiens
pmid	sentence
12510059	Insulin also activates jnk, erk, pkc and mtor, which induce the phosphorylation of irs1 on serine residues 307, 612 and 632 and inhibit its functions. Our results indicate that the insulin-stimulated degradation of irs-1 via the phosphatidylinositol 3-kinase pathway is in part dependent upon the ser(312) phosphorylation of irs-1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, AMPK Signaling, Insulin Signaling, Luminal Breast Cancer, Leptin Signaling, MTOR Signaling

Identifier	Residue	Organism
SIGNOR-270159		Homo sapiens
pmid	sentence
19767751	These results indicate that phosphorylation of nup153 and nup214 by erk strongly reduces their affinity for importin-. nup153 depletion caused a strong inhibition of nuclear accumulation of gfp?importin-beta in both erk-inhibited and erk-activated cells (fig. 8b,c), indicating that nup153 is essential for the efficient importin-beta transport.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-270200		in vitro
pmid	sentence
11287604	Plc beta1 could be efficiently phosphorylated by activated mitogen-activated protein kinase but not by pka. The erk phosphorylation site was mapped to serine 982

Publications:

1

Organism:

In Vitro

Pathways:

Oxytocin signaling

Identifier	Residue	Organism
SIGNOR-270137		Homo sapiens
pmid	sentence
10197981	Ras signaling was shown previously to induce the phosphorylation of the bmp mediator smad1 at four erk consensus sites in the linker domain (kretzschmar et al. 1997a). Phosphorylation of these four sites inhibits smad1 accumulation in the nucleus

Publications:

1

Organism:

Homo Sapiens

Tissue:

Lung, Breast

Identifier	Residue	Organism
SIGNOR-233526		Homo sapiens
pmid	sentence
23616010	Erk also undergoes rapid translocation into the nucleus, where it phosphorylates and activates a variety of transcription factor targets, including sp1, e2f, elk-1, and ap1.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Luminal Breast Cancer, Malignant Melanoma, Pancreatic ductal adenocarcinoma (PDA)

Identifier	Residue	Organism
SIGNOR-261214		Mus musculus
pmid	sentence
24663380	Ano6 deficiency significantly reduces ERK/AKT phosphorylation. Our data have also shown that Ano6-KD significantly attenuates ERK phosphorylation, which is implicated in the regulation of cancer cell proliferation by Ano1, suggesting that Ano6 is potentially involved in regulating myoblast proliferation through the ERK signaling pathway.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-270201		Homo sapiens
pmid	sentence
19237534	We previously established that phosphorylation of lsf in early g1 at ser-291 and ser-309 inhibits its transcriptional activity and that dephosphorylation later in g1 is required for its reactivation. At the peak activities of erk and cyclin c/cdk2 in early g1, lsf is efficiently phosphorylated on ser-291 and ser-309.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269927		Homo sapiens
pmid	sentence
12840032	P-erk1/2 proteins were efficiently dephosphorylated in vitro by protein phosphatases 1 and 2a (pp1/2a) and mapk phosphatase 3 (mkp3). the dual specificity phosphatases that specifically dephosphorylate and inactivate the p-erk1/2 are called mapk phosphatases

Publications:

1

Organism:

Homo Sapiens

Pathways:

Noonan syndrome

Identifier	Residue	Organism
SIGNOR-269922		Homo sapiens
pmid	sentence
16456541	B56-containing pp2a dephosphorylate erk and their activity is controlled by the early gene iex-1 and erk

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244662		Homo sapiens
pmid	sentence
20974802	We show that several proline-directed mitogen-activated protein kinases (mapks), such as p38, erk1/2, and jnk1 are sufficient and required for the phosphorylation of ppps/tp motifs of lrp6.

Publications:

1

Organism:

Homo Sapiens

Pathways:

WNT/FLT3

Identifier	Residue	Organism
SIGNOR-270145		Homo sapiens
pmid	sentence
15950189	Erk phosphorylates threonine 42 residue of ribosomal protein s3.

Publications:

1

Organism:

Homo Sapiens

Name	ERK1/2 View Modifications
Primary ID	SIGNOR-PF1
Type	protein family
Formed by	MAPK1, MAPK3
Relations	328
Pathways	Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, AMPK Signaling, B-cell activation, COVID-19 Causal Network, Colorectal Carcinoma, EGFR Signaling, Eosinophil: IL5, ErbB receptors in cancer, FAP: PDGFR alpha, FLT3-ITD in AML, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Insulin Signaling, Inhibition of Apoptosis, Integrin Signaling, Luminal Breast Cancer, Leptin Signaling, Mast cell: SCF, Mitochondrial dynamics in T cell exhaustion, Malignant Melanoma, Monocyte: IL10 transcriptional regulation, Monocyte: Macrophage differentiation, MTOR Signaling, Nucleotide Biosynthesis, Triple mutant AML, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Oxytocin signaling, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, SARS-CoV MAPK PERTURBATION, Satellite: CCR2, Thyroid cancer, T cell activation, Toll like receptors, T-Lymphocyte: IL6, T-Lymphocyte: TGF beta, VEGF Signaling, WNT/FLT3

The SIGnaling Network
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