Relation Results

Identifier	Residue	Sequence	Organism
SIGNOR-98384	Ser104	FSFDTDRsPAPMSCD	Homo sapiens
pmid	sentence
12591950	Biml (bim long) was induced and phosphorylated parallel to jnk activitythese data demonstrate that biml is phosphorylated in vivo on thr-56 and that jnk also phosphorylates biml on at least one serine residue (ser-44 and/or ser-58)

Identifier	Residue	Sequence	Organism
SIGNOR-98388	Ser118	DKSTQTPsPPCQAFN	Homo sapiens
pmid	sentence
12591950	Biml (bim long) was induced and phosphorylated parallel to jnk activitythese data demonstrate that biml is phosphorylated in vivo on thr-56 and that jnk also phosphorylates biml on at least one serine residue (ser-44 and/or ser-58)

Identifier	Residue	Sequence	Organism
SIGNOR-98392	Thr116	SCDKSTQtPSPPCQA	Homo sapiens
pmid	sentence
12591950	Biml (bim long) was induced and phosphorylated parallel to jnk activitythese data demonstrate that biml is phosphorylated in vivo on thr-56 and that jnk also phosphorylates biml on at least one serine residue (ser-44 and/or ser-58)

Publications:

3

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277642	Ser138	SLQLGAVsPGTLTPT	Homo sapiens	U2-OS Cell
pmid	sentence
21364637	JNK phosphorylates YAP on multiple sites. The wild-type YAP (WT) and five mutant (T119A, S138A, T154A, S317A and T362A) Flag–YAP constructs were each transfected into U2OS cells

Identifier	Residue	Sequence	Organism
SIGNOR-277644	Ser367	GTQNPVSsPGMSQEL	Homo sapiens
pmid	sentence
21364637	JNK phosphorylates YAP on multiple sites. The wild-type YAP (WT) and five mutant (T119A, S138A, T154A, S317A and T362A) Flag–YAP constructs were each transfected into U2OS cells

Identifier	Residue	Sequence	Organism
SIGNOR-277645	Ser400	SRDESTDsGLSMSSY	Homo sapiens
pmid	sentence
21364637	JNK phosphorylates YAP on multiple sites. The wild-type YAP (WT) and five mutant (T119A, S138A, T154A, S317A and T362A) Flag–YAP constructs were each transfected into U2OS cells

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277641	Thr119	AGTAGALtPQHVRAH	Homo sapiens	U2-OS Cell
pmid	sentence
21364637	JNK phosphorylates YAP on multiple sites. The wild-type YAP (WT) and five mutant (T119A, S138A, T154A, S317A and T362A) Flag–YAP constructs were each transfected into U2OS cells

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277643	Thr154	VVSGPAAtPTAQHLR	Homo sapiens	U2-OS Cell
pmid	sentence
21364637	JNK phosphorylates YAP on multiple sites. The wild-type YAP (WT) and five mutant (T119A, S138A, T154A, S317A and T362A) Flag–YAP constructs were each transfected into U2OS cells

Publications:

5

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-264063	Ser176	CTERFVSsPEEVMDV	Homo sapiens
pmid	sentence
27013971	JNK phosphorylates KIF5C on S176 in the motor domain; a site that we show is phosphorylated in brain. In the peroxisome cargo-bound state, S176 phosphorylated KIF5C(1-560) transports to microtubule plus ends, whereas dephosphorylated KIF5C(1-560) is bound tightly to microtubules resulting in an immobile state. As a consequence, phosphorylation of S176 can facilitate plus-end cargo transport by KIF5C(1-560).

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Sequence	Organism
SIGNOR-105758	Ser216	ILDLISEsPIKGRAQ	Homo sapiens
pmid	sentence
11259409	Using modified jnk and its atp analogue enables the detection of novel jnk substrates. Among substrates identified using this approach is heterogeneous nuclear ribonucleoprotein k, which is involved in transcription and post-transcriptional mrna metabolism. The newly identified substrate can be phosphorylated by jnk on amino acids 216 and 353, which contribute to heterogeneous nuclear ribonucleoprotein k mediated transcriptional activities.

Identifier	Residue	Sequence	Organism
SIGNOR-105762	Ser353	DSAIDTWsPSEWQMA	Homo sapiens
pmid	sentence
11259409	Using modified jnk and its atp analogue enables the detection of novel jnk substrates. Among substrates identified using this approach is heterogeneous nuclear ribonucleoprotein k, which is involved in transcription and post-transcriptional mrna metabolism. The newly identified substrate can be phosphorylated by jnk on amino acids 216 and 353, which contribute to heterogeneous nuclear ribonucleoprotein k mediated transcriptional activities.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252953	Ser230	PEGATPTsPVGHFAK	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252954	Thr227	PAPPEGAtPTSPVGH	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252955	Thr451	PIPKALGtPVLTPPT	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-252956	Thr455	ALGTPVLtPPTEAAS	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Publications:

4

Organism:

Homo Sapiens

Tissue:

Skin

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-168754	Ser230	PEGATPTsPVGHFAK	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-168758	Thr227	PAPPEGAtPTSPVGH	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-168762	Thr451	PIPKALGtPVLTPPT	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-168766	Thr455	ALGTPVLtPPTEAAS	Homo sapiens	Melanoma Cell
pmid	sentence
20959475	Braf(v600e) signaling through mitogen-activated protein kinase/extracellular signal-regulated kinase kinase resulted in increased reactive oxygen species levels and c-jun nh(2) terminal kinase-mediated activation of foxo4 via its phosphorylation on thr(223), ser(226), thr(447), and thr(451).

Publications:

4

Organism:

Homo Sapiens

Tissue:

Skin

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-235777	Ser312	TESITATsPASMVGG	Rattus norvegicus	H4-II-E-C3 Cell
pmid	sentence
12510059	Modulation of insulin-stimulated degradation of human insulin receptor substrate-1 by Serine 312 phosphorylationOne of the specific Ser phosphorylation sites in IRS-1 that has been proposed to negatively modulate the insulin signal is Ser312 (numbered according to the human sequence). Prior studies have demonstrated that IRS-1 associates with and is phosphorylated by JNK in vitro on Ser312

Publications:

1

Organism:

Rattus Norvegicus

Identifier	Residue	Sequence	Organism
SIGNOR-165026	Ser37	YLDSGIHsGATTTAP	Homo sapiens
pmid	sentence
20419129	Specifically, we provide evidence that jnk binds to e-cadherin/beta-catenin complex and phosphorylates beta-catenin at serine 37 and threonine 41, the sites also phosphorylated by gsk-3beta.

Identifier	Residue	Sequence	Organism
SIGNOR-187578	Ser37	YLDSGIHsGATTTAP	Homo sapiens
pmid	sentence
19667122	Specifically, we provide evidence that jnk binds to e-cadherin/beta-catenin complex and phosphorylates beta-catenin at serine 37 and threonine 41, the sites also phosphorylated by gsk-3beta.

Identifier	Residue	Sequence	Organism
SIGNOR-187582	Thr41	GIHSGATtTAPSLSG	Homo sapiens
pmid	sentence
19667122	Specifically, we provide evidence that jnk binds to e-cadherin/beta-catenin complex and phosphorylates beta-catenin at serine 37 and threonine 41, the sites also phosphorylated by gsk-3beta.

Publications:

3

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-99215	Ser62	PSWHLADsPAVNGAT	Homo sapiens	Prostate Gland Cancer Cell
pmid	sentence
12633850	We have identified that serine 62 is the necessary site for taxol- or 2-me-induced bcl-xl phosphorylation in summary, our studies suggest that the phosphorylation of bcl-xl by stress response kinase signaling might oppose the anti-apoptotic function of bcl-xl

Identifier	Residue	Sequence	Organism
SIGNOR-73638	Thr115	LTSQLHItPGTAYQS	Homo sapiens
pmid	sentence
10617621	Sapk phosphorylates bcl-x(l) on threonine 47 (thr-47) and threonine 115 (thr-115) in vitro and in vivo. In contrast to wild-type bcl-x(l), a mutant bcl-x(l) with the two threonines substituted by alanines (ala-47, ala-115) is a more potent inhibitor of ionizing radiation-induced apoptosis

Identifier	Residue	Sequence	Organism
SIGNOR-73642	Thr47	GTESEMEtPSAINGN	Homo sapiens
pmid	sentence
10617621	Sapk phosphorylates bcl-x(l) on threonine 47 (thr-47) and threonine 115 (thr-115) in vitro and in vivo. In contrast to wild-type bcl-x(l), a mutant bcl-x(l) with the two threonines substituted by alanines (ala-47, ala-115) is a more potent inhibitor of ionizing radiation-induced apoptosis

Publications:

3

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-260758	Ser63	KNSDLLTsPDVGLLK	Homo sapiens	HuH-7 Cell
pmid	sentence
21561061	3b Induces Phosphorylation of c-Jun (Ser-63) throughActivation of the JNK Pathway.\| An enhanced phosphorylation of JNK and MEK4 was observed in cells expressing 3b ascompared to control cells expressing GFP

Identifier	Residue	Sequence	Organism
SIGNOR-53784	Ser63	KNSDLLTsPDVGLLK	Homo sapiens
pmid	sentence
17158707	The JNK-mediated phosphorylation of both Ser63 and Ser73 within the transactivation domain of c-Jun (Table _(Table1)1) potentiates its transcriptional activity

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-236130	Ser63	KNSDLLTsPDVGLLK	Homo sapiens	Neuron
pmid	sentence
12040039	Stress in primary cultured cns neurons induces phosphorylation of c-jun serines 63 and 73 and increased c-jun protein. Jnk2/3 activity selectively targets c-jun.

Identifier	Residue	Sequence	Organism
SIGNOR-36466	Ser73	VGLLKLAsPELERLI	Homo sapiens
pmid	sentence
17158707	The JNK-mediated phosphorylation of both Ser63 and Ser73 within the transactivation domain of c-Jun (Table _(Table1)1) potentiates its transcriptional activity

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-236149	Ser73	VGLLKLAsPELERLI	Homo sapiens	Neuron
pmid	sentence
12040039	Stress in primary cultured cns neurons induces phosphorylation of c-jun serines 63 and 73 and increased c-jun protein. Thus, neuronal stress selectively activates JNK2/3 in the presence of mechanisms maintaining constitutive JNK1 activity, and this JNK2/3 activity selectively targets c-Jun, which is isolated from constitutive JNK1 activity.

Identifier	Residue	Sequence	Organism
SIGNOR-53788	Ser73	VGLLKLAsPELERLI	Homo sapiens
pmid	sentence
9405416	Phosphorylation by activated jnk protects c-jun from ubiquitination.

Publications:

6

Organism:

Homo Sapiens

Pathways:

TGF-beta Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-261133	Ser70	RDPVARTsPLQTPAA	in vitro
pmid	sentence
11323415	JNK1 directly phosphorylates Bcl2 at Ser70 in vitro and co-localizes with Bcl2 in mitochondrial membranes in vivo.

Publications:

1

Organism:

In Vitro

Pathways:

COVID-19 Causal Network, FLT3-ITD signaling, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Sequence	Organism
SIGNOR-137627	Thr69	SVIVADQtPTPTRFL	Homo sapiens
pmid	sentence
15916964	Phosphorylation of atf2 by jnk/p38 on thr69/71 is prerequisite to its transcriptional activities

Identifier	Residue	Sequence	Organism
SIGNOR-137631	Thr71	IVADQTPtPTRFLKN	Homo sapiens
pmid	sentence
15916964	Phosphorylation of atf2 by jnk/p38 on thr69/71 is prerequisite to its transcriptional activities

Publications:

2

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling

Identifier	Residue	Organism
SIGNOR-269984		Homo sapiens
pmid	sentence
15767678	Phosphoamino acid analysis confirmed that jnk caused thr phosphorylation of jip3 (fig. _(fig.3c).3c). This phosphorylation on thr was markedly decreased when thr266, thr276, and thr287 were replaced with ala. These data indicate that jnk phosphorylated jip3 on thr266, thr276, and thr287 in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269981		Homo sapiens
pmid	sentence
18553930	Specific phosphorylation of pp2czeta at ser (92) by stress-activated jnk attenuates its phosphatase activity in cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269978		Homo sapiens
pmid	sentence
12812981	Dentatorubral-pallidoluysian atrophy protein is phosphorylated by c-jun nh2-terminal kinase. serine 734 of the drpla protein is a phospho-acceptor site by jnk. The phosphorylation may be coupled to the activation of a protease. The molecular size of drpla protein detected in the rat brain with the specific phosphopeptide antibody was 150_kda, which was slightly smaller than that expected from the sequence and the results with the human protein. The phosphorylated forms of ha-tagged human drpla gradually disappeared after osmotic treatment,

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Organism
SIGNOR-269985		Homo sapiens
pmid	sentence
14699954	The targets of jnk include the transcription factors p53. P75ntr-mediated apoptosis was shown to be dependent of p53

Publications:

1

Organism:

Homo Sapiens

Pathways:

EBV infection, FLT3-ITD signaling

Identifier	Residue	Organism
SIGNOR-269982		Homo sapiens
pmid	sentence
20630875	Involved in the regulation of the microtubule (mt) filament system by destabilizing microtubules. Prevents assembly and promotes disassembly of microtubules. Here we show that in response to hyperosmotic stress, jnk phosphorylates a key cytoplasmic microtubule regulatory protein, stathmin (stmn), on conserved ser-25 and ser-38 residues. In in vitro biochemical studies, we identified stmn ser-38 as the critical residue required for efficient phosphorylation by jnk and identified a novel kinase interaction domain in stmn required for recognition by jnk. We revealed that jnk was required for microtubule stabilization in response to hyperosmotic stress.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269884		Homo sapiens
pmid	sentence
18922779	Bi-78d3, dose-dependently inhibits the phosphorylation of jnk substrates both in vitro and in cell.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269886		Homo sapiens
pmid	sentence
15767678	The c-jun nh2-terminal kinase (jnk)-interacting protein (jip) group of scaffold proteins (jip1, jip2, and jip3) can interact with components of the jnk signaling pathway and potently activate jnk.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269887		Homo sapiens
pmid	sentence
10903733	Overexpression of bcma activates jnk

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-253340		Homo sapiens
pmid	sentence
24315690	In addition to the possible regulation of the transcription factor c-Jun by phosphorylation via the c-Jun N-terminal kinase (JNK) or the kinases ERK1, ERK2 and GSK3β, further signaling pathways lead to an up-regulation of c-Jun protein and thus AP-1 activity

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling

Identifier	Residue	Organism
SIGNOR-261929		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-83729		Homo sapiens
pmid	sentence
11062067	Here we report that mkk4 shows a striking preference for the tyrosine residue (tyr-185), and mkk7 a striking preference for the threonine residue (thr-183) in three sapk1/jnk1 isoforms tested (jnk1 alpha 1, jnk2 alpha 2 and jnk3 alpha 1).

Identifier	Residue	Organism	Cell Line
SIGNOR-236110		Homo sapiens	COS-7 Cell
pmid	sentence
8974401	A MAP kinase kinase kinase (MAPKKK), termed ASK1, was identified that activated two different subgroups of MAP kinase kinases (MAPKK), SEK1 (or MKK4) and MKK3/MAPKK6 (or MKK6), which in turn activated stress-activated protein kinase (SAPK, also known as JNK; c-Jun amino-terminal kinase) and p38 subgroups of MAP kinases, respectively.

Identifier	Residue	Organism	Cell Line
SIGNOR-260759		Homo sapiens	HuH-7 Cell
pmid	sentence
21561061	Activation of JNK pathway components in 3b-expressing cells was assessed by analyzing levels of active phosphorylated formsof JNK and its upstream kinase MEK4. An enhanced phosphor-ylation of JNK and MEK4 was observed in cells expressing 3b ascompared to control cells expressing GFP

Publications:

3

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling

Identifier	Residue	Organism
SIGNOR-267617		Homo sapiens
pmid	sentence
26428373	AP1 is a dimeric transcription factor composed of members of the Jun and Fos protooncoprotein families. AP1 was found induced by LMP1 through the JNK signaling cascade, involving JNK1-mediated phosphorylation and activation of c-Jun. JNK1 activation critically relies on CTAR2 and its P379VQLSYY motif. It has long been unclear which signaling mediators at CTAR2 are involved in JNK activation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

EBV infection

Identifier	Residue	Organism
SIGNOR-261131		Chlorocebus aethiops
pmid	sentence
15294014	Furthermore, N expression up-regulated the activity of stress-activated protein kinases, namely the JNK and p38 MAPK pathways.

Publications:

1

Organism:

Chlorocebus Aethiops

Pathways:

COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism
SIGNOR-260760		Homo sapiens
pmid	sentence
21561061	An enhanced phosphorylation of JNK and MEK4 was observed in cells expressing 3b ascompared to control cells expressing GFP

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION

Identifier	Residue	Organism
SIGNOR-260178		Homo sapiens
pmid	sentence
18931691	JNKs activate apoptotic signaling by the upregulation pro-apoptotic genes via the transactivation of specific transcription factors or by directly modulating the activities of mitochondrial pro- and anti-apoptotic proteins through distinct phosphorylation events.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, SARS-CoV MAPK PERTURBATION, SARS-CoV ER STRESS

Identifier	Residue	Organism	Cell Line
SIGNOR-269883		Homo sapiens	Macrophage
pmid	sentence
9625767	Il-1 binding to its receptor triggers a cascade of signaling events, including activation of the stress-activated mitogen-activated protein (map) kinases, c-jun nh2-terminal kinase (jnk) and p38 map kinase, as well as transcription factor nuclear factor kappab (nf-kappab

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-260177		Homo sapiens
pmid	sentence
31226023	The kinase activity of IRE1 also activates a signaling cascade that ultimately activates c-Jun N-terminal kinase (JNK)

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, SARS-CoV ER STRESS

Identifier	Residue	Organism
SIGNOR-269885		Homo sapiens
pmid	sentence
11717429	We report the identification of an anthrapyrazolone series with significant jnk1, -2, and -3 (k(i) = 0.19 microm). To determine whether jnk activity is required for stress-induced translocation of bax to the mitochondria, we examined the effect of sp600125, a jnk inhibitor.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269977		Homo sapiens
pmid	sentence
15071501	Demonstrate that jnk-mediated phosphorylation of 14-3-3 induces the release of bax from 14-3-3 and triggers its translocation to the mitochondria; these results strongly indicate that jnk regulates the activity of bax by phosphorylating 14-3-3 proteins.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, FLT3-ITD signaling

Identifier	Residue	Organism
SIGNOR-269980		Homo sapiens
pmid	sentence
15071501	Jnk phosphorylates 14-3-3zetaat ser-184 and 14-3-3sigmaat ser-190

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-269979		Homo sapiens
pmid	sentence
15071501	Here we demonstrate that activated jnk promotes bax translocation to mitochondria through phosphorylation of 14-3-3, a cytoplasmic anchor of bax. Phosphorylation of 14-3-3 led to dissociation of bax from this protein.Jnk phosphorylates 14-3-3zeta_ at ser-184 and 14-3-3sigma_ at ser-191

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-83725		Homo sapiens
pmid	sentence
11062067	Here we report that MKK4 shows a striking preference for the tyrosine residue (Tyr-185), and MKK7 a striking preference for the threonine residue (Thr-183) in three SAPK1/JNK1 isoforms tested (JNK1 alpha 1, JNK2 alpha 2 and JNK3 alpha 1).

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network

Identifier	Residue	Organism
SIGNOR-269983		Homo sapiens
pmid	sentence
20220133	Here we show that jnk directly phosphorylates cdc25c at serine 168 during g(2) phase of the cell cycle. Cdc25c phosphorylation by jnk negatively regulates its phosphatase activity and thereby cdk1 activation, enabling a timely control of mitosis onset.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-236113		Homo sapiens	Mv1Lu Cell
pmid	sentence
10601313	JNK-mediated phosphorylation of Smad3 outside the -SSXS motif enhances Smad3 nuclear translocation and potentiates transcriptional activation independent of Smad3 phosphorylation by T_RI.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, TGF-beta Signaling

Identifier	Residue	Organism
SIGNOR-205437		Homo sapiens
pmid	sentence
25290089	The irak1/traf6 complex can also activate jnk and p38 signalling through assembly of a catalytically active tab2-tab3-tak1 complex.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-205449		Homo sapiens
pmid	sentence
25290089	The irak1/traf6 complex can also activate jnk and p38 signalling through assembly of a catalytically active tab2-tab3-tak1 complex.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-262214		Homo sapiens
pmid	sentence
26095609	ANXA3 Induces a Feed-Forward Loop that Is Mediated by the MKK4/JNK Signaling Cascade. To substantiate the importance of the JNK/AP-1 pathway in ANXA3-driven HCC, we performed rescue experiments using the JNK-specific inhibitor (JNKi) SP600125. JNKi suppressed the oncogenic properties conferred by ANXA3 overexpression, as evidenced by the diminished abilities of HCC cells to form colonies, migrate, invade, induce angiogenesis, form hepatospheres, and resist apoptosis and chemotherapy (Figures 6F–6J). Interestingly, treatment of parental HCC cells or HCC cells overexpressing ANXA3 with JNKi resulted in not only a reduction in JNK activity and modulation of downstream target genes (c-MYC and p21) but also a marked decrease in ANXA3 expression, suggesting that ANXA3 induces a feed-forward loop that is mediated by MKK4/JNK signaling (Figures 6K–6L).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-262216		Homo sapiens	Hepatoma Cell
pmid	sentence
26095609	ANXA3 Induces a Feed-Forward Loop that Is Mediated by the MKK4/JNK Signaling Cascade. To substantiate the importance of the JNK/AP-1 pathway in ANXA3-driven HCC, we performed rescue experiments using the JNK-specific inhibitor (JNKi) SP600125. JNKi suppressed the oncogenic properties conferred by ANXA3 overexpression, as evidenced by the diminished abilities of HCC cells to form colonies, migrate, invade, induce angiogenesis, form hepatospheres, and resist apoptosis and chemotherapy (Figures 6F–6J). Interestingly, treatment of parental HCC cells or HCC cells overexpressing ANXA3 with JNKi resulted in not only a reduction in JNK activity and modulation of downstream target genes (c-MYC and p21) but also a marked decrease in ANXA3 expression, suggesting that ANXA3 induces a feed-forward loop that is mediated by MKK4/JNK signaling (Figures 6K–6L).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-205443		Homo sapiens
pmid	sentence
25290089	The irak1/traf6 complex can also activate jnk and p38 signalling through assembly of a catalytically active tab2-tab3-tak1 complex.

Publications:

1

Organism:

Homo Sapiens

Name	JNK View Modifications
Primary ID	SIGNOR-PF15
Type	protein family
Formed by	MAPK10, MAPK8, MAPK9
Relations	66
Pathways	COVID-19 Causal Network, IBD_DENDRITIC CELLS, EBV infection, FLT3-ITD signaling, IBD_IEC, Macrophage: IL1 beta, SARS-CoV MAPK PERTURBATION, SARS-CoV ER STRESS, TGF-beta Signaling, YAP/TAZ regulation

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