Relation Results

Identifier	Residue	Sequence	Organism
SIGNOR-244975	Ser122	DGRMVQLsPPALAAP	Homo sapiens
pmid	sentence
11904294	We found that hypoxia greatly accelerated tal1 turnover in these cells through mitogen-activated protein kinase (mapk)2-mediated phosphorylation, ubiquitination, and proteasomal degradation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-244784	Ser307	TRRSRTEsITATSPA	Homo sapiens
pmid	sentence
11160134	Thus, at least three kinases mediate phosphorylation of ser307, including jnk, serine kinases in the pi 3-kinase cascade that are activated byinsulinor igf-1, and mek1-sensitive kinase cascades during tnf-alfa stimulation.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Muscle

Pathways:

Adipogenesis, Insulin Signaling, Luminal Breast Cancer

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276674	Ser329	DVNAGEGsEFADSGI	Homo sapiens	HEK-293T Cell
pmid	sentence
25124033	Phosphorylation of Ser329, Ser334, and Thr340 in Tiam1 is required for its interaction with βTrCP1. The proteolysis of Tiam1 is prevented by βTrCP silencing, inhibition of CK1 and MEK, or mutation of the Tiam1 degron site.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244792	Thr185	HDHTGFLtEYVATRW	Homo sapiens	BJ Cell
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.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-244788	Tyr187	HTGFLTEyVATRWYR	Homo sapiens	BJ Cell
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.

Identifier	Residue	Organism
SIGNOR-258990		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-244795		Homo sapiens	Adipocyte
pmid	sentence
12270934	Mek1 as indicated by extensive phosphorylation of erk1 and erk2 during the initial 2 h of adipogenesis.

Publications:

4

Organism:

Homo Sapiens, Mus Musculus

Identifier	Residue	Sequence	Organism
SIGNOR-244802	Thr202	HDHTGFLtEYVATRW	Homo sapiens
pmid	sentence
9677429	The mek1 proline-rich insert is required for efficient activation of the mitogen-activated protein kinases erk1 and erk2 in mammalian cells.

Identifier	Residue	Sequence	Organism
SIGNOR-244806	Tyr204	HTGFLTEyVATRWYR	Homo sapiens
pmid	sentence
9677429	The mek1 proline-rich insert is required for efficient activation of the mitogen-activated protein kinases erk1 and erk2 in mammalian cells.

Identifier	Residue	Organism
SIGNOR-244798		Homo sapiens
pmid	sentence
12270934	Mek1 as indicated by extensive phosphorylation of erk1 and erk2 during the initial 2 h of adipogenesis.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-244780	Tyr216	RGEPNVSyICSRYYR	Homo sapiens
pmid	sentence
15020233	In vitro kinase assay was carried out using a recombinant human active mek1 and we found that gsk-3beta was phosphorylated on tyr(216) by this kinase in a dose- and time-dependent manner. Further, the pretreatment of fibroblasts with u0126 inhibited serum-induced nuclear translocation of gsk-3beta. These results suggested that mek1/2 induces tyrosine phosphorylation of gsk-3beta and this cellular event might induce nuclear translocation of gsk-3beta.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Skin

Pathways:

Adipogenesis, Acute Myeloid Leukemia, AML_TRIPLETS, FLT3-ITD signaling, Insulin Signaling, PI3K/AKT Signaling

Identifier	Residue	Organism
SIGNOR-244854		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-263059		Homo sapiens
pmid	sentence
28138032	Mechanistically, Ras-MEK signaling drives Chk1 expression and promotes cancer cell growth that produces genotoxic stress that requires Chk1 to mediate a response to the consequent DNA damage. Reciprocally, Chk1 engages a negative feedback loop to prevent hyperactivation of Ras-MEK signaling, thereby limiting DNA damage. Ras–MEK signaling transcriptionally activates Chk1, which appears to sustain cancer cell growth by maintaining DNA damage levels below a threshold that would otherwise drive apoptosis.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Organism
SIGNOR-244945		Homo sapiens
pmid	sentence
11018021	The best characterized Raf substrates are MEK1 and MEK2. The activation of MEK1/2 by Raf is required to mediate many of the cellular responses to Raf activation, suggesting that MEK1/2 are the dominant Raf effector proteins.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Ovary

Pathways:

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

Identifier	Residue	Organism
SIGNOR-244971		Homo sapiens
pmid	sentence
18596912	The genomic activity of ppargamma is modulated, in addition to ligand binding, by phosphorylation of a serine residue by mapks, such as extracellular signal-regulated protein kinases-1/2 (erk-1/2), or by nucleocytoplasmic compartmentalization through the erk activators mapk kinases-1/2 (mek-1/2). These mapks phosphorylate (in humans) ser 84 in the ppargamma1 and ser 114 in ppargamma2 isoform.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Rett syndrome, Thyroid cancer

Identifier	Residue	Organism
SIGNOR-244827		Mus musculus
pmid	sentence
8131746	Activation of mek family kinases requires phosphorylation of two conserved ser/thr residueserine residues 218 and 222 of human mek1 are the primary sites for phosphorylation by c-raf.

Identifier	Residue	Organism
SIGNOR-244831		in vitro
pmid	sentence
8413257	Raf-1 phosphorylation of MEK activated it, as judged by its ability to stimulate the phosphorylation of myelin basic protein by glutathione S-transferase-ERK1.

Identifier	Residue	Organism
SIGNOR-251988		Homo sapiens
pmid	sentence
21900390	BRAFV600E has been shown to initiate thyroid follicular cell transformation. The BRAFV600E mutation disrupts the hydrophobic interaction, enabling the BRAF kinase to fold into a catalytically active formation, resulting in an almost 500-fold increase in kinase activity. Mutant BRAF can dimerize and activate MEK without Ras activation.

Publications:

3

Organism:

Mus Musculus, In Vitro, 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
SIGNOR-244892		Homo sapiens
pmid	sentence
8131746	Activation of mek family kinases requires phosphorylation of two conserved ser/thr residues.Phosphopeptide analysis demonstrated that serine residues 218 and 222 of human mek1 are the primary sites for phosphorylation by c-raf

Identifier	Residue	Organism	Cell Line
SIGNOR-244904		Homo sapiens	HEK-293 Cell
pmid	sentence
15466476	Cot proteins were used in an in vitro kinase assay using mek as a substrate. Samples were analyzed by western blotting. As seen in the cascade activity assay only wild-type cot was active against mekregulation of cot is of great interest to the signaling field since the cot/mek/erk pathway potentially plays a role in the etiology of inflammatory autoimmune diseases.

Publications:

2

Organism:

Homo Sapiens

Pathways:

Toll like receptors

Identifier	Residue	Organism	Cell Line
SIGNOR-244920		Homo sapiens	HeLa Cell
pmid	sentence
16129686	Inhibition of pak kinase activity dramatically decreased phosphorylation of mek1 at ser(298) in response to either pdgf or egf.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-244934		Homo sapiens	HEK-293 Cell
pmid	sentence
15175348	In vitro kinase assay revealed that the direct targets of pdk1 in the mapk pathway were the upstream mapk kinases mek1 and mek2. The identified pdk1 phosphorylation sites in mek1 and mek2 are ser222 and ser226, respectively, and are known to be essential for full activation

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, B-cell activation, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, Insulin Signaling, Luminal Breast Cancer, Malignant Melanoma, Non-small-cell lung cancer (NSCLC), PI3K/AKT Signaling, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-244874		Homo sapiens
pmid	sentence
15547943	We analyzed the ability of mp1 to bind to mek1, erk1, and to itself, and the regulation of these interactions. Gel filtration of cell lysates revealed two major mp1 peaks: a broad high molecular weight peak and a 28 kda complex. An mp1 mutant that lost mek1 binding no longer enhanced rasv12-stimulated erk1 activity, and functioned as a dominant negative, consistent with the concept that mp1 function depends on facilitating these oligomerizations.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-244930		Homo sapiens	Neuron
pmid	sentence
11160424	The mek1/2 inhibitors pd98059, sl327, and u0126 have been extensively used to implicate erk1/2 in neuroplasticity.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Organism	Cell Line
SIGNOR-263511		Homo sapiens	Skin Fibroblast
pmid	sentence
12839928	Activation of p38 MAPK is required for arsenite-induced apoptosis and MEK1,2 dephosphorylation in human skin fibroblasts. Our data suggest the presence of a continuous negative feedback from p38α and p38β to MEK1,2 as simultaneous inhibition of p38α and p38β isoforms in normal quiescent cells resulted in accumulation of phosphorylated MEK1,2 (Fig. 2A) ⇓ . This negative regulation of MEK1,2 in normal cells could be considered a means to control MEK1,2-mediated proliferation and expression of transformation-related genes.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling, Toll like receptors

Identifier	Residue	Organism
SIGNOR-244941		Homo sapiens
pmid	sentence
20626350	In particular, p38 mapk activity stimulates the physical association between ppa2 and mkk1/2- erk1/2 complex, leading to mkk1/2 dephosphorilation by pp2a.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, PI3K/AKT Signaling

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-244865		Homo sapiens
pmid	sentence
12270934	Fibroblast growth factor-2 (FGF-2), in the presence of dexamethasone, isobutylmethylxanthine, and insulin, induces a prolonged activation of the MEK/ERK signaling pathway, which lasts for at least 12 h post-induction, and this activity is less sensitive to the MEK inhibitors

Publications:

1

Organism:

Homo Sapiens

Pathways:

Luminal Breast Cancer

Identifier	Residue	Organism
SIGNOR-244888		Homo sapiens
pmid	sentence
11343802	Both mekk2 and mekk3 are able to activate the jun kinase pathway in vivo. However, following routine immunoprecipitation in triton x-100, mekk2 but not mekk3 is able to effectively phosphorylate both sek-1 and mek-1 and to undergo autophosphorylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-244912		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

Identifier	Residue	Organism	Cell Line
SIGNOR-244916		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.

Publications:

2

Organism:

Homo Sapiens, Chlorocebus Aethiops

Identifier	Residue	Organism
SIGNOR-259446		Homo sapiens
pmid	sentence
26347206	Trametinib (Mekinist™) is a reversible and highly selective allosteric inhibitor of MEK1 and MEK2 with anticancer activity against metastatic melanoma carrying the BRAF V600 mutation.

Identifier	Residue	Organism	Cell Line
SIGNOR-262312		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:

2

Organism:

Homo Sapiens

Pathways:

SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism
SIGNOR-244823		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Pathways:

SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism	Cell Line
SIGNOR-244868		Mus musculus	3T3-L1 Cell
pmid	sentence
12270934	Fibroblast growth factor-2 (FGF-2), in the presence of dexamethasone, isobutylmethylxanthine, and insulin, induces a prolonged activation of the MEK/ERK signaling pathway, which lasts for at least 12 h post-induction, and this activity is less sensitive to the MEK inhibitors

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Organism
SIGNOR-244809		Homo sapiens
pmid	sentence
21779497	Active raf phosphorylates mek.

Identifier	Residue	Organism	Cell Line
SIGNOR-244813		Homo sapiens	HeLa Cell
pmid	sentence
8621729	Our data demonstrated that a-raf is, indeed, a mek1 activator and may play a role in growth factor signaling.

Publications:

2

Organism:

Homo Sapiens

Pathways:

EGFR Signaling

Identifier	Residue	Organism
SIGNOR-263069		Homo sapiens
pmid	sentence
28138032	Mechanistically, Ras-MEK signaling drives Chk1 expression and promotes cancer cell growth that produces genotoxic stress that requires Chk1 to mediate a response to the consequent DNA damage. Reciprocally, Chk1 engages a negative feedback loop to prevent hyperactivation of Ras-MEK signaling, thereby limiting DNA damage. Ras–MEK signaling transcriptionally activates Chk1, which appears to sustain cancer cell growth by maintaining DNA damage levels below a threshold that would otherwise drive apoptosis.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Organism
SIGNOR-244938		Homo sapiens
pmid	sentence
15175348	The identified pdk1 phosphorylation sites in mek1 and mek2 are ser222 and ser226, respectively, and are known to be essential for full activation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, B-cell activation, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, Insulin Signaling, Luminal Breast Cancer, Malignant Melanoma, Non-small-cell lung cancer (NSCLC), PI3K/AKT Signaling, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-244952		Homo sapiens
pmid	sentence
11018021	The best characterized Raf substrates are MEK1 and MEK2. The activation of MEK1/2 by Raf is required to mediate many of the cellular responses to Raf activation, suggesting that MEK1/2 are the dominant Raf effector proteins.

Publications:

1

Organism:

Homo Sapiens

Pathways:

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

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

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.

Publications:

2

Organism:

Homo Sapiens, Chlorocebus Aethiops

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-269913		Homo sapiens
pmid	sentence
12270934	Mek1 as indicated by extensive phosphorylation of erk1 and erk2 during the initial 2 h of adipogenesis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244924		Homo sapiens
pmid	sentence
12876277	We find that adhesion to fibronectin induces pak1-dependent phosphorylation of mek1 on s298 and that this phosphorylation is necessary for efficient activation of mek1 and subsequent mapk activation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, T cell activation, Toll like receptors

Identifier	Residue	Organism	Cell Line
SIGNOR-244955		Homo sapiens	Neuron
pmid	sentence
11160424	The mek1/2 inhibitors pd98059, sl327, and u0126 have been extensively used to implicate erk1/2 in neuroplasticity

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Organism	Cell Line
SIGNOR-263512		Homo sapiens	Skin Fibroblast
pmid	sentence
12839928	Activation of p38 MAPK is required for arsenite-induced apoptosis and MEK1,2 dephosphorylation in human skin fibroblasts. Our data suggest the presence of a continuous negative feedback from p38α and p38β to MEK1,2 as simultaneous inhibition of p38α and p38β isoforms in normal quiescent cells resulted in accumulation of phosphorylated MEK1,2 (Fig. 2A) ⇓ . This negative regulation of MEK1,2 in normal cells could be considered a means to control MEK1,2-mediated proliferation and expression of transformation-related genes.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244820		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244958		Homo sapiens
pmid	sentence
9873633	The mek1/2 inhibitors pd98059, sl327, and u0126 have been extensively used to implicate erk1/2 in neuroplasticity. u0126 was found to functionally antagonize ap-1 transcriptional activity via noncompetitive the dual specificity kinase mek with an ic50 of 0.07 microm for mek 1 and 0.06 microm for mek 2.

Publications:

1

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Organism
SIGNOR-244961		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244877		Homo sapiens
pmid	sentence
18481201	Pd98059, a specific inhibitor of mek 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:

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-244881		Mus musculus	NIH-3T3 Cell
pmid	sentence
8131746	Phosphorylation at ser-218 and ser-222 by map kinase kinase kinases (raf or mekk1) positively regulates mek1 kinase activity.

Publications:

1

Organism:

Mus Musculus

Pathways:

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

Identifier	Residue	Organism	Cell Line
SIGNOR-244773		Mus musculus	3T3-L1 Cell
pmid	sentence
12270934	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, NPM1_new

Identifier	Residue	Organism	Cell Line
SIGNOR-262210		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-244847		Homo sapiens
pmid	sentence
8114697	P34cdc2 catalyzes the in vitro phosphorylation of mkk1 on both of these threonine residues and inactivates mkk1 enzymatic activity. Both sites are phosphorylated in vivo as well

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, KIT in AML

Identifier	Residue	Organism
SIGNOR-244964		Homo sapiens
pmid	sentence
15118098	Morg1 specifically associates with several components of the erk pathway, including mp1, raf-1, mek, and erk, and stabilizes their assembly into an oligomeric complex.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244871		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Pathways:

SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism
SIGNOR-244927		Homo sapiens
pmid	sentence
Other

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	Cell Line
SIGNOR-275410		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-258991		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-244843		Homo sapiens
pmid	sentence
8668348	We show that, consequently, b-raf interacts with mek-1 and mek-2 with a better affinity than does c-raf-1, thus strengthening the notion that b-raf is a stronger mek activator than c-raf-l.

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-270222
pmid	sentence
12792650	Inhibition of caspase-9 through phosphorylation at Thr 125 by ERK MAPK\|The opposing protein kinase activity is overcome by treatment with the broad-specificity kinase inhibitor staurosporine or with inhibitors of MEK1/2

Publications:

1

Pathways:

COVID-19 Causal Network, Inhibition of Apoptosis

Name	MEK1/2 View Modifications
Primary ID	SIGNOR-PF25
Type	protein family
Formed by	MAP2K1, MAP2K2
Relations	62
Pathways	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, Mitochondrial dynamics in T cell exhaustion, 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

The SIGnaling Network
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