| + |
UBE2I | down-regulates activity 
sumoylation
|
JUN |
0.43 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263002 |
Lys226 |
HPRLQALkEEPQTVP |
Homo sapiens |
|
| pmid |
sentence |
| 16055711 |
We report here that lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229. Sumoylation of c-Fos preferentially occurs in the context of c-Jun/c-Fos heterodimers.|Inhibition of c-Fos and c-Jun sumoylation stimulates AP-1-dependent transcription activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263001 |
Lys254 |
MESQERIkAERKRMR |
Homo sapiens |
|
| pmid |
sentence |
| 16055711 |
We report here that lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229. Sumoylation of c-Fos preferentially occurs in the context of c-Jun/c-Fos heterodimers.|Inhibition of c-Fos and c-Jun sumoylation stimulates AP-1-dependent transcription activity. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
SAE1/SAE2 complex | down-regulates activity
sumoylation
|
JUN |
0.257 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263006 |
Lys226 |
HPRLQALkEEPQTVP |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 16055711 |
We report here that lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229. Sumoylation of c-Fos preferentially occurs in the context of c-Jun/c-Fos heterodimers.|Inhibition of c-Fos and c-Jun sumoylation stimulates AP-1-dependent transcription activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263005 |
Lys254 |
MESQERIkAERKRMR |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 16055711 |
We report here that lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229. Sumoylation of c-Fos preferentially occurs in the context of c-Jun/c-Fos heterodimers.|Inhibition of c-Fos and c-Jun sumoylation stimulates AP-1-dependent transcription activity. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
DYRK2 | down-regulates
phosphorylation
|
JUN |
0.259 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-195771 |
Ser243 |
PGETPPLsPIDMESQ |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 22307329 |
Degradation of c-jun/c-myc is a critical process for the g(1)/s transition, which is initiated upon phosphorylation by glycogen synthase kinase 3 ? (gsk3?). However, a specific kinase or kinases responsible for priming phosphorylation events that precede this gsk3? Modification has not been definitively identified. Here, we found that the dual-specificity tyrosine phosphorylation-regulated kinase dyrk2 functions as a priming kinase of c-jun and c-myc.The finding that kinase-active dyrk2 phosphorylated gst_c-jun210_310-wt by detection with an anti_phospho_c-jun(ser243) antibody demonstrated that dyrk2 is a ser243 kinase in vitro |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GSK3B | down-regulates activity
phosphorylation
|
JUN |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235892 |
Ser243 |
PGETPPLsPIDMESQ |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16023596 |
The c-jun and c-myc oncogenic transcription factors are highly unstable proteins due to polyubiquitination. Similar to c-myc, we report here that phosphorylation of c-jun by gsk3 creates a high-affinity binding site for the e3 ligase fbw7, which targets c-jun for polyubiquitination and proteasomal degradation similar to c-myc, we report here that phosphorylation of c-jun by gsk3 creates a high-affinity binding site for the e3 ligase fbw7, which targets c-jun for polyubiquitination and proteasomal degradation.Phosphorylation of Thr-239 and Ser-243 is required for Fbw7-mediated c-Jun disappearance |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-18684 |
Ser249 |
LSPIDMEsQERIKAE |
in vitro |
|
| pmid |
sentence |
| 1846781 |
Phosphorylation of recombinant human c-jun proteins in vitro by gsk-3 decreases their dna-binding activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236717 |
Thr239 |
VPEMPGEtPPLSPID |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16023596 |
The c-jun and c-myc oncogenic transcription factors are highly unstable proteins due to polyubiquitination. Similar to c-myc, we report here that phosphorylation of c-jun by gsk3 creates a high-affinity binding site for the e3 ligase fbw7, which targets c-jun for polyubiquitination and proteasomal degradation similar to c-myc, we report here that phosphorylation of c-jun by gsk3 creates a high-affinity binding site for the e3 ligase fbw7, which targets c-jun for polyubiquitination and proteasomal degradation.Phosphorylation of Thr-239 and Ser-243 is required for Fbw7-mediated c-Jun disappearance |
|
| Publications: |
3 |
Organism: |
Homo Sapiens, In Vitro |
| Pathways: | Acute Myeloid Leukemia, Insulin Signaling, WNT/FLT3 |
| + |
PP2B | up-regulates 
dephosphorylation
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152006 |
Ser243 |
PGETPPLsPIDMESQ |
Homo sapiens |
Neuron, A-431 Cell |
| pmid |
sentence |
| 17215518 |
Importantly, pp2b not only dephosphorylates the c-jun at ser-243 but also interacts with c-jun in pma-treated cells. Pma stimulates the association of the pp2b/c-jun/sp1 complex with the promoter. These findings indicate the dephosphorylation of c-jun c terminus is required for the c-jun/sp1 interaction |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GSK3A | down-regulates
phosphorylation
|
JUN |
0.338 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-21776 |
Ser243 |
PGETPPLsPIDMESQ |
Homo sapiens |
|
| pmid |
sentence |
| 1846781 |
Phosphorylation of recombinant human c-jun proteins in vitro by gsk-3 decreases their dna-binding activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-21780 |
Ser249 |
LSPIDMEsQERIKAE |
Homo sapiens |
|
| pmid |
sentence |
| 1846781 |
Phosphorylation of recombinant human c-jun proteins in vitro by gsk-3 decreases their dna-binding activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-21784 |
Thr239 |
VPEMPGEtPPLSPID |
Homo sapiens |
|
| pmid |
sentence |
| 1846781 |
Phosphorylation of recombinant human c-jun proteins in vitro by gsk-3 decreases their dna-binding activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-138592 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16023596 |
Similar to c-myc, we report here that phosphorylation of c-jun by gsk3 creates a high-affinity binding site for the e3 ligase fbw7, which targets c-jun for polyubiquitination and proteasomal degradation. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
CSNK2A1 | down-regulates
phosphorylation
|
JUN |
0.574 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-19603 |
Ser249 |
LSPIDMEsQERIKAE |
Homo sapiens |
|
| pmid |
sentence |
| 1516134 |
Casein kinase ii is a negative regulator of c-jun dna binding and ap-1 activitywe show that two of these sites, thr-231 and ser-249, are phosphorylated by casein kinase ii (ckii). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-19607 |
Thr231 |
ALKEEPQtVPEMPGE |
Homo sapiens |
|
| pmid |
sentence |
| 1516134 |
Casein kinase ii is a negative regulator of c-jun dna binding and ap-1 activitywe show that two of these sites, thr-231 and ser-249, are phosphorylated by casein kinase ii (ckii). |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PRKDC |
phosphorylation
|
JUN |
0.415 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248934 |
Ser249 |
LSPIDMEsQERIKAE |
in vitro |
|
| pmid |
sentence |
| 8464713 |
Here, we show that the DNA-PK modifies c-Jun in vitro and that serine residue 249 (Ser-249) is required for phosphorylation to occur. This residue corresponds to one of three sites of c-Jun that are phosphorylated in vivo and which negatively regulate c-Jun DNA binding in vitro. However, we find that phosphorylation of c-Jun by the DNA-PK does not interfere with DNA binding, indicating that phosphorylation at other sites is required for this effect. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
HRAS | up-regulates activity
phosphorylation
|
JUN |
0.516 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236682 |
Ser63 |
KNSDLLTsPDVGLLK |
Rattus norvegicus |
Fibroblast |
| pmid |
sentence |
| 1749429 |
Expression of oncogenic ha-ras augments transactivation by c-jun and stimulates its phosphorylation. Here we describe the mapping of the ha-ras-responsive phosphorylation sites to serines 63 and 73 of c-jun. Site-directed mutagenesis indicates that phosphorylation of these serines is essential for stimulation of c-jun activity and for cooperation with ha-ras in ocogenic transformation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235522 |
Ser63 |
KNSDLLTsPDVGLLK |
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 12169099 |
c-Jun was first shown to be phosphorylated in its transactivation domain (Ser-63 and Ser-73) by ERKs and p54-JNK. This is consistent with other studies which show that PD98059 inhibits up-regulation of c-Jun protein in Ras-transformed NIH-3T3 cells |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236686 |
Ser73 |
VGLLKLAsPELERLI |
Rattus norvegicus |
Fibroblast |
| pmid |
sentence |
| 1749429 |
Expression of oncogenic ha-ras augments transactivation by c-jun and stimulates its phosphorylation. Here we describe the mapping of the ha-ras-responsive phosphorylation sites to serines 63 and 73 of c-jun. Site-directed mutagenesis indicates that phosphorylation of these serines is essential for stimulation of c-jun activity and for cooperation with ha-ras in ocogenic transformation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235526 |
Ser73 |
VGLLKLAsPELERLI |
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 12169099 |
c-Jun was first shown to be phosphorylated in its transactivation domain (Ser-63 and Ser-73) by ERKs and p54-JNK. This is consistent with other studies which show that PD98059 inhibits up-regulation of c-Jun protein in Ras-transformed NIH-3T3 cells |
|
| Publications: |
4 |
Organism: |
Rattus Norvegicus, Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl, EGFR Signaling, Glioblastoma Multiforme, Insulin Signaling |
| + |
MAPK9 | up-regulates
phosphorylation, binding
|
JUN |
0.881 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183017 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 19118012 |
Phosphorylation by activated jnk protects c-jun from ubiquitination;phosphorylation of c-jun on ser73 by jnk is sufficient to protect c-jun from ubiquitination c-jun is targeted for ubiquitination by its association with inactive c-jun nh2-terminal kinase (jnk). Phosphorylation by activated jnk protects c-jun from ubiquitination, thus by prolonging its half-life targets of the jnk signal transduction pathway include the transcription factors atf2 and c-jun apoptosis, altered;apoptosis, induced;transcription, altered;cell growth, altered;jnk1(disrupts);pin1(induces);dna(disrupts) transcription, altered;cell growth, altered;jnk1(disrupts);pin1(induces);dna(disrupts) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-88208 |
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 |
Cell Line |
| SIGNOR-88212 |
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. Jnk2/3 activity selectively targets c-jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-53791 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9405416 |
C-jun is targeted for ubiquitination by its association with inactive c-jun nh2-terminal kinase (jnk).Phosphorylation By activated jnk protects c-jun from ubiquitination. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
JNK | up-regulates activity
phosphorylation
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| 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-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 |
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 |
Cell Line |
| SIGNOR-53788 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 9405416 |
Phosphorylation by activated jnk protects c-jun from ubiquitination. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| 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. |
|
| Publications: |
6 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
CDK3 | up-regulates
phosphorylation
|
JUN |
0.455 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183009 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 19118012 |
Egf-induced cdk3 activation caused c-jun phosphorylation at ser63 and ser73, resulting in increased ap-1 transactivation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183013 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 19118012 |
Egf-induced cdk3 activation caused c-jun phosphorylation at ser63 and ser73, resulting in increased ap-1 transactivation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
VRK1 | up-regulates
phosphorylation
|
JUN |
0.528 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-127069 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 15378002 |
Vrk1 phosphorylates c-jun in ser63 and ser73 in vitro...VRK1 Activates c-jun dependent transcription |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-127073 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 15378002 |
Vrk1 phosphorylates c-jun in ser63 and ser73 in vitro...VRK1 Activates c-jun dependent transcription |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
MAPK15 | up-regulates
phosphorylation
|
JUN |
0.44 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-91371 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 12169099 |
Up-regulation of c-jun mrna in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-jun n-terminal kinases are required for efficient up-regulation of c-jun protein. these data suggest that erks, rather than jnks, are required for c- jun up-regulation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-91375 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 12169099 |
Up-regulation of c-jun mrna in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-jun n-terminal kinases are required for efficient up-regulation of c-jun protein. these data suggest that erks, rather than jnks, are required for c- jun up-regulation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PLK3 | up-regulates
phosphorylation
|
JUN |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-157721 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 17804415 |
Stress-induced c-jun activation mediated by polo-like kinase 3 in corneal epithelial cells. Hypoxia/reoxygenation activated plk3 in hce cells to directly phosphorylate c-jun proteins at phosphorylation sites ser-63 and ser-73, and to increase dna binding activity of c-jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-179551 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 18650425 |
Stress-induced c-jun activation mediated by polo-like kinase 3 in corneal epithelial cells. Hypoxia/reoxygenation activated plk3 in hce cells to directly phosphorylate c-jun proteins at phosphorylation sites ser-63 and ser-73, and to increase dna binding activity of c-jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-179555 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 18650425 |
Stress-induced c-jun activation mediated by polo-like kinase 3 in corneal epithelial cells. Hypoxia/reoxygenation activated plk3 in hce cells to directly phosphorylate c-jun proteins at phosphorylation sites ser-63 and ser-73, and to increase dna binding activity of c-jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-157725 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 17804415 |
Stress-induced c-jun activation mediated by polo-like kinase 3 in corneal epithelial cells. Hypoxia/reoxygenation activated plk3 in hce cells to directly phosphorylate c-jun proteins at phosphorylation sites ser-63 and ser-73, and to increase dna binding activity of c-jun. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
MAPK3 | up-regulates
phosphorylation
|
JUN |
0.774 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-91379 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 12169099 |
Up-regulation of c-jun mrna in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-jun n-terminal kinases are required for efficient up-regulation of c-jun protein. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-91383 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 12169099 |
Up-regulation of c-jun mrna in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-jun n-terminal kinases are required for efficient up-regulation of c-jun protein. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
MAPK8 | up-regulates activity
phosphorylation
|
JUN |
0.905 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235766 |
Ser63 |
KNSDLLTsPDVGLLK |
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 8137421 |
The jnk-mediated phosphorylation of both ser63 and ser73 within the transactivation domain of c-jun potentiates its transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250122 |
Ser73 |
VGLLKLAsPELERLI |
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 8137421 |
JNK1 binds to the c-Jun transactivation domain and phosphorylates it on Ser-63 and Ser-73. The effect on AP-1 transcriptional activity results, in part, from enhanced phosphorylation of the c-Jun NH2-terminal activation domain. |
|
| Publications: |
2 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | Acute Myeloid Leukemia, EGFR Signaling, Glucocorticoid receptor Signaling, SAPK/JNK Signaling, TNF-alpha Signaling, WNT Signaling, WNT/FLT3, WNT Signaling and Myogenesis |
| + |
MAPK10 | up-regulates
phosphorylation
|
JUN |
0.883 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164800 |
Ser63 |
KNSDLLTsPDVGLLK |
Homo sapiens |
|
| pmid |
sentence |
| 20395206 |
With epidermal growth factor treatment, overexpression of erk8 in jb6 cl41 cells caused an increased phosphorylation of c-jun at ser(63) and ser(73), resulting in increased activator protein-1 transactivation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164804 |
Ser73 |
VGLLKLAsPELERLI |
Homo sapiens |
|
| pmid |
sentence |
| 20395206 |
With epidermal growth factor treatment, overexpression of erk8 in jb6 cl41 cells caused an increased phosphorylation of c-jun at ser(63) and ser(73), resulting in increased activator protein-1 transactivation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PAK2 | up-regulates
phosphorylation
|
JUN |
0.272 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170760 |
Thr2 |
tAKMETTF |
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 21177766 |
P21-activated protein kinase (pak2)-mediated c-jun phosphorylation at 5 threonine sites promotes cell transformationour data showed that pak2 binds and phosphorylates c-jun at five threonine sites (thr2, thr8, thr89, thr93 and thr286) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170764 |
Thr286 |
RLEEKVKtLKAQNSE |
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 21177766 |
P21-activated protein kinase (pak2)-mediated c-jun phosphorylation at 5 threonine sites promotes cell transformationour data showed that pak2 binds and phosphorylates c-jun at five threonine sites (thr2, thr8, thr89, thr93 and thr286) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170768 |
Thr8 |
MTAKMETtFYDDALN |
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 21177766 |
P21-activated protein kinase (pak2)-mediated c-jun phosphorylation at 5 threonine sites promotes cell transformationour data showed that pak2 binds and phosphorylates c-jun at five threonine sites (thr2, thr8, thr89, thr93 and thr286) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170772 |
Thr89 |
QSSNGHItTTPTPTQ |
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 21177766 |
P21-activated protein kinase (pak2)-mediated c-jun phosphorylation at 5 threonine sites promotes cell transformationour data showed that pak2 binds and phosphorylates c-jun at five threonine sites (thr2, thr8, thr89, thr93 and thr286) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170776 |
Thr93 |
GHITTTPtPTQFLCP |
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 21177766 |
P21-activated protein kinase (pak2)-mediated c-jun phosphorylation at 5 threonine sites promotes cell transformationour data showed that pak2 binds and phosphorylates c-jun at five threonine sites (thr2, thr8, thr89, thr93 and thr286) |
|
| Publications: |
5 |
Organism: |
Homo Sapiens |
| + |
ABL1 |
phosphorylation
|
JUN |
0.542 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-245370 |
Tyr170 |
LHSEPPVyANLSNFN |
Homo sapiens |
|
| pmid |
sentence |
| 10637231 |
After phosphorylation of c-Jun by Abl on Tyr170, both proteins interacted via the SH2 domain of Abl |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ABL1 | up-regulates activity
phosphorylation
|
JUN |
0.542 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251428 |
Tyr170 |
LHSEPPVyANLSNFN |
in vitro |
|
| pmid |
sentence |
| 10637231 |
Active nuclear Abl efficiently phosphorylate c-Jun. After phosphorylation of c-Jun by Abl on Tyr170, both proteins interacted via the SH2 domain of Abl. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
SMAD3/SMAD4 | up-regulates activity
binding
|
JUN |
0.702 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-229545 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9732876 |
Smad3 and smad4 also act together with c-jun and c-fos to activate transcription in response to tgf-beta, through a tgf-beta-inducible association of c-jun with smad3 and an interaction of smad3 and c-fos |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
ERK1/2 | up-regulates activity
phosphorylation
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
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 |
| + |
Cullin 1-RBX1-Skp1 | down-regulates quantity by destabilization
polyubiquitination
|
JUN |
0.392 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272949 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 14739463 |
We report that in neurons the stability of c-Jun is regulated by the E3 ligase SCF(Fbw7), which ubiquitinates phosphorylated c-Jun and facilitates c-Jun degradation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | form complex 
binding
|
SMAD4/JUN |
0.663 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-51110 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9312063 |
Our analysis of the regulation of dpc4 transcriptional activity by c-jun was consistent with the possibility that c-jun and dpc4 could interact and produce trans-activation of the 3tp-lux reporter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | form complex
binding
|
AP1 |
0.951 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256365 |
|
|
in vitro |
|
| pmid |
sentence |
| 3142692 |
The c-Jun and c-fos proto-oncogenes encode proteins that form a complex which regulates transcription from promoters containing AP-1 activation elements. c-Jun has specific DNA binding activity, while c-Fos has homology to the putative DNA binding domain of c-Jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256361 |
|
|
in vitro |
|
| pmid |
sentence |
| 2467839 |
The protein products of the fos (Fos) and jun (Jun) proto-oncogenes have been shown to associate with a DNA element known as the transcription factor activator protein-1 (AP-1) binding site. Jun (previously known as the Fos-binding protein p39) and Fos form a protein complex in the nucleus. These data demonstrate a cooperative interaction between the protein products of two proto-oncogenes with a DNA element involved in transcriptional regulation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256363 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1904542 |
The proteins encoded by the proto-oncogenes c-fos and c-jun (Fos and Jun, respectively) form a heterodimeric complex that regulates transcription by interacting with the DNA-regulatory element known as the activator protein 1 (AP-1) binding site. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256367 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25875593 |
C-Fos dimerizes with c-Jun to form the transcription activator protein-1 (AP-1) which binds to the specific recognition site. |
|
| Publications: |
4 |
Organism: |
In Vitro, Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, Luminal Breast Cancer, SARS-CoV CYTOKINE STORM, TGF-beta Signaling |
| + |
JUN | form complex
binding
|
SMAD3/JUN |
0.741 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-59867 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9732876 |
These results show a ligand-dependent association of smad3 with c-jun |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
(-)-anisomycin | up-regulates
chemical activation
|
JUN |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-189632 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates quantity by expression 
transcriptional regulation
|
CYP19A1 |
0.35 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254876 |
|
|
Homo sapiens |
Endometrial Cancer Cell Line |
| pmid |
sentence |
| 19022561 |
We found that both SF1 and LRH1 can transcriptionally cooperate with the AP-1 family members c-JUN and c-FOS, known to be associated with enhanced proliferation of endometrial carcinoma cells, to further enhance activation of the STAR, HSD3B2, and CYP19A1 PII promoters. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Luminal Breast Cancer |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
JUN |
0.572 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256065 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 17041602 |
Knockdown of the transcription factor PU.1 (encoded by Sfpi1) leads to acute myeloid leukemia (AML) in mice. We examined the transcriptome of preleukemic hematopoietic stem cells (HSCs) in which PU.1 was knocked down (referred to as 'PU.1-knockdown HSCs') to identify transcriptional changes preceding malignant transformation. Transcription factors c-Jun and JunB were among the top-downregulated targets. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, HaematopoiesisTranscriptionalControl |
| + |
JDP2 | down-regulates activity
binding
|
JUN |
0.627 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-226398 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18671972 |
JDP2 dimerizes with other AP-1 proteins such as activating transcription factor-2 (ATF2) and Jun to repress transcription from promoters that contain a cyclic AMP-responsive element (CRE). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates
binding
|
TCF4 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-138544 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16007074 |
Phosphorylation-dependent interaction between c-jun and tcf4;c-jun and tcf4 cooperatively activated the c-jun promoter in reporter assays |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | WNT/FLT3 |
| + |
TLR4 | up-regulates activity
|
JUN |
0.456 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249518 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 19592489 |
The transcription factor AP-1 consists of a variety of dimers composed of members of the Jun, Fos, and ATF families of proteins. The Jun proteins can both homo- and heterodimerize with Fos members to form transcriptionally active complexes. The stimulation of macrophage TLR4 receptor rapidly activates not only the NF-kappaB pathway but also MAPK pathways, including JNK, ERK, and p38. Many of the downstream targets of MAPK pathways are transcription factors that include c-Jun. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
HSD3B2 |
0.274 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254874 |
|
|
Homo sapiens |
Endometrial Cancer Cell Line |
| pmid |
sentence |
| 19022561 |
We found that both SF1 and LRH1 can transcriptionally cooperate with the AP-1 family members c-JUN and c-FOS, known to be associated with enhanced proliferation of endometrial carcinoma cells, to further enhance activation of the STAR, HSD3B2, and CYP19A1 PII promoters. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RNF7 | down-regulates activity
ubiquitination
|
JUN |
0.331 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271452 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23136067 |
SAG (Sensitive to Apoptosis Gene), also known as RBX2 (RING box protein 2), ROC2 (Regulator of Cullins 2), or RNF7 (RING Finger Protein 7), was originally cloned in our laboratory as a redox inducible antioxidant protein and later characterized as the second member of the RBX/ROC RING component of the SCF (SKP1-CUL-F-box Proteins) E3 ubiquitin ligase. by forming a complex with other components of the SCF E3 ligase, SAG promotes ubiquitination and degradation of a number of protein substrates, including c-JUN, DEPTOR, HIF-1α, IκBα, NF1, NOXA, p27, and procaspase-3, thus regulating various signaling pathways and biological processes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates
|
MTHFR |
0.276 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253147 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18065414 |
The induction of MTHFR was also observed after overexpression of inositol-requiring enzyme-1 (IRE1) and was inhibited by a dominant-negative mutant of IRE1. Because IRE1 triggers c-Jun signaling, we examined the possible involvement of c-Jun in up-regulation of MTHFR. Transfection of c-Jun and two activators of c-Jun (LiCl and sodium valproate) increased MTHFR expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DUSP1 | down-regulates activity
dephosphorylation
|
JUN |
0.467 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277102 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26734995 |
However, adenovirus mediated overexpression of MKP-1 only slightly decreased JNK and c-Jun phosphorylation compared with the severe inactivation of JNK activities induced by MKK7 knockdown.|The results suggested that HDACI-induced MKP-1 contributes to inactivation of JNK instead of ERK, consistent with the previous reports in other cell types |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
JUN |
0.733 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251679 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8639160 |
We have described how the receptor uses several means to achieve repression of the genes regulated by AP-1 and NF-KB proteins |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
FOSL1 |
0.82 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261604 |
|
|
Homo sapiens |
HBE Cell |
| pmid |
sentence |
| 13679379 |
Members of the AP1 family distinctly regulated the fra-1 promoter. In particular, coexpression of c-Jun, Jun-D, and Fra-2 up-regulated fra-1 transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
LORICRIN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254536 |
|
|
Homo sapiens |
Keratinocyte |
| pmid |
sentence |
| 12200429 |
Mutation and DNA-protein analyses show that Sp1, c-Jun, an unidentified regulator, and the co-activator p300/CREB-binding protein up-regulate whereas Sp3, CREB-1/CREMalpha/ATF-1, Jun B, and an AP2-like protein (termed the keratinocyte-specific repressor-1 (KSR-1)) suppress loricrin promoter activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEF2C | up-regulates quantity by expression
transcriptional regulation
|
JUN |
0.605 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-47139 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9069290 |
One consequence of mef2c activation is increased c-jun gene transcription. Our results show that p38 may influence host defence and inflammation by maintaining the balance of c-jun protein consumed during infection |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | down-regulates activity
binding
|
SMAD3 |
0.741 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256284 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10871633 |
These results indicate that interaction between Smad3 and c-Jun may repress Smad3 transcriptional activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SAPK/JNK Signaling, TGF-beta Signaling |
| + |
NfKb-p65/p50 | up-regulates
binding
|
JUN |
0.578 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216337 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18174238 |
Chromatin immunoprecipitation (chip) analysis confirmed the serum-induced recruitment of jund to the promoter in vivo and showed that the presence of jund was dependent on the presence of p65 and p50, indicating a protein-protein-dependent mechanism of jund recruitment |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Glucocorticoid receptor Signaling, SARS-CoV CYTOKINE STORM, TNF-alpha Signaling |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
TGFB1 |
0.524 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251713 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 23936544 |
MAPKs have cis-acting regulatory elements in the mouse-TGF promoter region, which respond to various transcription factors, including specificity protein-1 and activating protein 1. Thus, it is possible that apoptotic cell-induced TGF-beta mRNA expression is mediated through activation of these transcription factors via MAPK signaling. Xiao et al. reported that all of the MAPK members, including p38/ERK/JNK, are required for apoptotic Jurkat cells up-regulation of TGF-beta production |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | TGF-beta Signaling |
| + |
CREB5 | up-regulates activity
binding
|
JUN |
0.522 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-240397 |
|
|
in vitro |
|
| pmid |
sentence |
| 8440710 |
CRE-BPa binds to CRE with higher affinity than to the 12-O-tetradecanoylphorbol-13-acetate response element as a homodimer or a CRE-BPa/c-Jun or CRE-BPa/CRE-BP1 heterodimer. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-219634 |
|
|
Chlorocebus aethiops |
CV-1 Cell |
| pmid |
sentence |
| 8378084 |
CRE-BPa specifically binds to CRE as a homodimer or heterodimer with c-Jun or CRE-BP1. In CAT cotransfection experiments using CV-1 cells, transient expression of each of four CRE-BPa proteins caused a 1.6- to 3.4-fold increase of CRE-dependent transcription |
|
| Publications: |
2 |
Organism: |
In Vitro, Chlorocebus Aethiops |
| + |
DCX DET1-COP1 | down-regulates quantity by destabilization
polyubiquitination
|
JUN |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271500 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 14739464 |
We report that human DET1 (hDET1) promotes ubiquitination and degradation of the proto-oncogenic transcription factor c-Jun by assembling a multisubunit ubiquitin ligase containing DNA Damage Binding Protein-1 (DDB1), cullin 4A (CUL4A), Regulator of Cullins-1 (ROC1), and constitutively photomorphogenic-1. Ablation of any subunit by RNA interference stabilized c-Jun and increased c-Jun-activated transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PPARG | up-regulates activity
|
JUN |
0.571 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249558 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 17681149 |
Transcriptional repression of inflammatory response genes occurs by negative interference of PPARg with the nuclear factor kB (NF-kB), signal transducer and activator of transcription (STAT), and activating protein 1 (AP-1) signaling pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | down-regulates 
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256560 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 12553907 |
In contrast, c-Jun is required for the survival of liver tumor cells. Reduced tumor formation strictly correlated with high apoptotic indices in c-Jun-deficient tumors, suggesting that increased apoptosis in c-Jun-deficient liver tumors is the primary cause for impaired tumorigenesis. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, TNF-alpha Signaling |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
RCAN1 |
0.28 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253148 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 18641051 |
Taken together, our findings suggest that c-Jun, a transcription factor downstream of the JNK signaling pathway, up-regulates Adapt78 expression in response to TG-induced ER stress and contributes to protection against TG-induced cell death. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
KRT16 |
0.271 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253905 |
|
|
Homo sapiens |
HaCaT Cell |
| pmid |
sentence |
| 12954631 |
these results suggest that Sp1 and AP1 sites in the essential promoter region are critical for EGF response, and Sp1 showed a functional cooperation with c-Jun and coactivators p300/CBP in driving the transcriptional regulation of EGF-induced keratin 16 gene expression. The coactivators p300/CBP could collaborate with Sp1 and c-Jun in the activation of keratin 16 promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RPL10 | down-regulates
binding
|
JUN |
0.397 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90750 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12138090 |
The qm gene encodes a 24.5 kda ribosomal protein l10 known to be highly homologous to a jun-binding protein (jif-1), which inhibits the formation of jun-jun dimers. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates
|
Brown_adipogenesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-198834 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22944199 |
Other g protein-mediated pathways are the planar cell polarity (pcp) pathway (shown in blue) leading to the activation of rac/rho, c-jun n-terminal kinase (jnk), and/or rho-associated kinase (rock). Jnk can induce jun, which, together with fos, forms the ap-1 early response transcription factor. Both pcp pathways have been implicated in cytoskeletal rearrangements |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle, Skeletal Muscle |
| Pathways: | WNT Signaling and Myogenesis |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
miR-155 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255767 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24708856 |
We found overexpression of miR-155 led to increase in cJUN, FOS and TRIB2, and decrease in MEIS1, GFI1, cMYC and JARID2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
CFI |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254787 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10630630 |
The production of CFI by Hep G2 cells was enhanced in a dose- and time-dependent fashion by 12-O-tetradecanoyl-1,2-phorbol 13-acetate (TPA), a potent PKC activator. The enhancement of the activity of transfected chimeric CAT constructs by TPA was abrogated by calphostin C and by pyrrolidine dithiocarbamate (an inhibitor of NF-kappaB and AP-1 transactivation). These results indicate that TPA regulation of CFI gene requires PKC signalling and is mediated by via a TPA response element (TRE) in the CFI promoter region located at -136/-130 and involves the transactivation of AP-1 and NF-kappaB transcription factors |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ARNT | down-regulates quantity by repression
transcriptional regulation
|
JUN |
0.554 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253697 |
|
|
Homo sapiens |
Hep-G2 Cell |
| pmid |
sentence |
| 21544813 |
Screening by quantitative reverse-transcription PCR and PCR arrays revealed that cyclin E1, CDK2, Fos and Jun were negatively regulated by ARNT, whereas CDKN1C, CNKN2A, CDKN2B, MAPK11 and MAPK14 were positively regulated in HCC |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
TNFAIP6 |
0.314 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254052 |
|
|
|
|
| pmid |
sentence |
| 8454627 |
Tumor necrosis factor (TNF)-stimulated gene 6 (TSG-6) encodes a protein expressed during inflammation. We have previously shown that transcription factors of the NF-IL6 and AP-1 families cooperatively modulate activation of the TSG-6 gene by TNF or interleukin 1 (IL-1) through a promoter region that contains an NF-IL6 site (-106 to -114) and an AP-1 element |
|
| Publications: |
1 |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
SERPINA3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254808 |
|
|
Homo sapiens |
Astrocyte Cell Line |
| pmid |
sentence |
| 11027208 |
We characterize a molecular mechanism responsible for both IL-1 and TNF-induced expression of ACT gene in astrocytes. We identify the 5' distal IL-1/TNF-responsive enhancer of the ACT gene located 13 kb upstream of the transcription start site. This 413-bp-long enhancer contains three elements, two of which bind nuclear factor kB (NF-kB) and one that binds activating protein 1 (AP-1). All of these elements contribute to the full responsiveness of the ACT gene to both cytokines, as determined by deletion and mutational analysis. The 5' NF-kB high-affinity binding site and AP-1 element contribute most to the enhancement of gene transcription in response to TNF and IL-1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FBXW7 | down-regulates quantity by destabilization
binding
|
JUN |
0.509 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272950 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 14739463 |
We report that in neurons the stability of c-Jun is regulated by the E3 ligase SCF(Fbw7), which ubiquitinates phosphorylated c-Jun and facilitates c-Jun degradation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
AML1-ETO | down-regulates activity
binding
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255670 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 12393465 |
Here we show that AML1-ETO blocks the transcriptional activity of PU.1 by displacing its coactivator c-Jun. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
| + |
Host translation inhibitor nsp1 | down-regulates activity
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262505 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 17715225 |
SARS-CoV nsp1 inhibits c-Jun expression and phosphorylation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
miR-155 | up-regulates quantity by expression
post transcriptional regulation
|
JUN |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255761 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24708856 |
We found overexpression of miR-155 led to increase in cJUN, FOS and TRIB2, and decrease in MEIS1, GFI1, cMYC and JARID2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
MUC12 | up-regulates activity
binding
|
JUN |
0.259 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265474 |
|
|
Homo sapiens |
Renal Cell Carcinoma Cell |
| pmid |
sentence |
| 32596961 |
MUC12 promoted the recruitment of c-Jun on the promoter of TGF-β1, leading to its transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HLX | up-regulates quantity by expression
transcriptional regulation
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261623 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20008130 |
In this study, we have identified cell cycle regulatory genes as downstream targets of the homeobox gene HLX in cultured trophoblast cells, namely RB1, MYC, EGR1, CDKN1C, ELK1, CCNB1, and JUN. RB1 and MYC mRNA expression was increased with HLX inactivation, whereas EGR1, CDKN1C, ELK1, CCNB1, and JUN mRNA expression was decreased compared with mock-transfected control cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
STAR |
0.262 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254875 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19022561 |
We found that both SF1 and LRH1 can transcriptionally cooperate with the AP-1 family members c-JUN and c-FOS, known to be associated with enhanced proliferation of endometrial carcinoma cells, to further enhance activation of the STAR, HSD3B2, and CYP19A1 PII promoters. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates activity
binding
|
SPI1 |
0.572 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255660 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 12393465 |
These results indicate that AML1-ETO competes c-Jun away from binding to the β3β4 domain of PU.1. Thus, the c-Jun coactivation function of PU.1 is down-regulated and this in turn down-regulates transcriptional activity of PU.1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, HaematopoiesisTranscriptionalControl |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
DDIT3 |
0.596 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254123 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 19299913 |
Promoter deletion and reporter analysis revealed that hypoxia transcriptionally activates a GADD153 promoter through the AP-1 element in neonatal cardiomyocytes. Ectopic overexpression of GADD153 resulted in the downregulation of CARP expression. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
ERK1/2 |
phosphorylation
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
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 |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252225 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16149046 |
Constitutively active mutants of activating transcription factor 2 (ATF2) and c-Jun additionally stimulated GTP cyclohydrolase I promoter activity, but to a lesser extent than the constitutively active CREB mutant. Enzymatic reactions that require tetrahydrobiopterin as cofactor are therefore indirectly controlled by signaling cascades involving the signal-responsive transcription factors CREB, c-Jun, and ATF2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DVL1 | up-regulates
binding
|
JUN |
0.472 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-178038 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 18347071 |
In this study, we discovered two novel interactions between dvl and c-jun and between dvl and beta-catenin in the nucleus that mediate the formation of a dvlc-junbeta-catenintcf functional complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, WNT Signaling, WNT/FLT3, WNT Signaling and Myogenesis |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
GLS |
0.358 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268035 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28111979 |
The transcription factor c-Jun can directly bind to the GLS gene promoter and enhance expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DDX21 | up-regulates activity
binding
|
JUN |
0.468 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260977 |
|
|
Homo sapiens |
HEK-293 Cell, HT-1080 Cell |
| pmid |
sentence |
| 11823437 |
C-Jun and RHII/Gu proteins interact in human cells at their endogenous level of expression. The helicase activity of RHII/Gu specifically facilitates c-Jun-mediated transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PML-RARalpha | up-regulates activity
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259940 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 8415704 |
PML-RAR alpha chimera cooperates with c-Jun and, strikingly, with c-Fos to stimulate the transcription of both synthetic and natural reporter genes containing an AP-1 site |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
MMP13 |
0.404 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254539 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20338993 |
The activated c-Jun protein has been proven to activate binding to the MMP-13 promoter and also upregulate the amount of MMP-13. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PELI3 | up-regulates
|
JUN |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-103989 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12874243 |
Pellino3 leads to activation of c-jun and elk-1, but not nf-kappab |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JUN | up-regulates
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-233467 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9878062 |
Functional data suggest that c-Jun is not merely a target for activation by many of the extracellular stimuli, but that it plays a role in mediating the cellular response. In the case of growth control, three lines of evidence suggest that the transcription factor AP-1, which is composed of FosJun and JunJun dimers, mediates cell proliferation in response to external growth signals in the form of peptide growth factors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, EGFR Signaling, Glioblastoma Multiforme, Glucocorticoid receptor Signaling, Insulin Signaling, Luminal Breast Cancer, TNF-alpha Signaling, TGF-beta Signaling, WNT Signaling, WNT/FLT3 |
| + |
JUN | up-regulates
|
Monocyte_differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256066 |
|
|
Mus musculus |
Hematopoietic Stem Cell |
| pmid |
sentence |
| 17041602 |
These results show that restoration of c-Jun expression rescues the myelomonocytic differentiation block in preleukemic PU.1-knockdown bone marrow cells, suggesting that c-Jun is a critical downstream target in PU.1-knockdown HSCs. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
JUN | up-regulates
|
Cell_migration |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-229760 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23151663 |
Planar cell polarity (PCP) signalling is prominently involved in the regulation of cell polarity, cell motility and morphogenetic movements, throught the activation of JUN transcription factor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | WNT Signaling |
| + |
RELA | up-regulates
binding
|
JUN |
0.708 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-160330 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18174238 |
Chromatin immunoprecipitation (chip) analysis confirmed the serum-induced recruitment of jund to the promoter in vivo and showed that the presence of jund was dependent on the presence of p65 and p50, indicating a protein-protein-dependent mechanism of jund recruitment |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
MAPK1 | up-regulates activity
phosphorylation
|
JUN |
0.784 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-201943 |
|
|
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: | Glucocorticoid receptor Signaling |
| + |
JUN | up-regulates activity
binding
|
SMAD4 |
0.663 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236139 |
|
|
Canis lupus familiaris |
|
| pmid |
sentence |
| 9312063 |
Our analysis of the regulation of dpc4 transcriptional activity by c-jun was consistent with the possibility that c-jun and dpc4 could interact and produce trans-activation of the 3tp-lux reporter. |
|
| Publications: |
1 |
Organism: |
Canis Lupus Familiaris |
| Pathways: | TGF-beta Signaling |
| + |
FOS | up-regulates activity
binding
|
JUN |
0.951 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252087 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 2516828 |
The cFos proto-oncoprotein associates with cJun to form a heterodimer with increased DNA binding and transcriptional activities. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, EGFR Signaling |
| + |
ERN1 | up-regulates
|
JUN |
0.394 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253146 |
|
|
Homo sapiens |
Neuro-2a Cell |
| pmid |
sentence |
| 18065414 |
The induction of MTHFR was also observed after overexpression of inositol-requiring enzyme-1 (IRE1) and was inhibited by a dominant-negative mutant of IRE1. Because IRE1 triggers c-Jun signaling, we examined the possible involvement of c-Jun in up-regulation of MTHFR. Transfection of c-Jun and two activators of c-Jun (LiCl and sodium valproate) increased MTHFR expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Gbeta | up-regulates
phosphorylation
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270033 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12169099 |
Up-regulation of c-jun mrna in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-jun n-terminal kinases are required for efficient up-regulation of c-jun protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NANOGP8 | down-regulates quantity by repression
transcriptional regulation
|
JUN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266091 |
|
|
Bluetongue virus (serotype 10 / American isolate) |
Keratinocyte |
| pmid |
sentence |
| 23839044 |
Constitutive NanogP8 overexpression in adult L1 mice reduced CD34+α6+ and Lrig-1+ bulge stem cells, impaired keratinocyte migration, and repressed the expression of many stem cell-associated genes, including Bmp5, Fgfr2, Jmjd1a, and Jun. |
|
| Publications: |
1 |
Organism: |
Bluetongue Virus (serotype 10 / American Isolate) |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
ABCB1 |
0.351 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254534 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 10369069 |
Co-transfection of WT cells with a c-jun expression vector and either of the AP-1 luciferase constructs demonstrated that c-jun could activate gene expression from both the consensus and the MDR1 AP-1 sites in a dose dependent manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD3/SMAD4 | down-regulates activity
|
JUN |
0.702 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249557 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 10973958 |
NF-kB-, AP-1-, and Smad3-driven promoters all require p300/CREB-binding protein for their transactivation. Previous studies have suggested that NF-kB- and AP-1-driven promoters can be inhibited by competitive recruitment of coactivators such as p300/CPB to other unrelated promoters. We hypothesized that NF-kB and AP-1 compete with Smad3 for limiting quantities of p300. This hypothesis predicts that added p300 should alleviate TGF-b1/Smad3-mediated inhibition of inflammatory genes. Conversely, increasing doses of TGF-b1/Smad3 would compete away even overexpressed p300 from NF-kB/AP- 1-driven promoters. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
3.0
JUN
- 
- 