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JUN — TP53
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Schreiber et al., Genes Dev 1999
:
Furthermore, the absence of c-Jun results in elevated expression of the tumor suppressor gene p53 and its target gene, the CDK inhibitor p21, whereas overexpression of
c-Jun represses
p53 and p21 expression and accelerates cell proliferation ... Rather,
c-Jun regulates transcription of
p53 negatively by direct binding to a variant AP-1 site in the p53 promoter
Kirch et al., Oncogene 1999
:
Expression of human
p53 requires synergistic activation of transcription from the p53 promoter by
AP-1 , NF-kappaB and Myc/Max
MacLaren et al., Oncogene 2000
:
Consistent with this latter observation, inhibition of
p53 function by HPV16 E6 protein
had no effect on
v-Jun induced cell death
She et al., Cancer Res 2001
:
We found that in a mouse JB6 epidermal cell line, resveratrol activated extracellular-signal regulated protein kinases ( ERKs ),
c-Jun NH2-terminal kinases (JNKs) , and p38 kinase and
induced serine 15 phosphorylation of
p53
Inamura et al., Brain Res 2001
:
In this study, we further investigated the role of
p53 in neuronal apoptosis, by examining whether caspases and
c-Jun N-terminal kinase (JNK) are
involved in the DNA strand break induced apoptosis
Jiang et al., Oncogene 2001
(Stomach Neoplasms) :
Functional
p53 is
required for triptolide induced apoptosis and
AP-1 and nuclear factor-kappaB activation in gastric cancer cells
Ahn et al., Cancer Lett 2002
(Skin Neoplasms) :
Inhibitory effect of glycolic acid on ultraviolet B-induced c-fos expression,
AP-1 activation and
p53-p21 response in a human keratinocyte cell line
Sun et al., J Cell Biochem 2004
:
We also demonstrate that both p300 and TATA box binding proteins cooperated with the transcription factor AP-1 to induce the promoter of MMP1 ; however,
p53 only inhibited the p300 mediated induction of the MMP1 promoter and the inhibition was
-72AP-1 dependent
Watanabe et al., Oncogene 2006
(Prostatic Neoplasms...) :
In RT112 and LNCap, CDDP
induced p53 and p21 expression, while pretreatment of dicoumarol suppressed induction of p53/p21 and resulted in sequential activation of
c-Jun N-terminal kinase (JNK) in a time dependent manner
Adam et al., Cancer Res 2009
(Neoplasms...) :
Furthermore, induction of
p53 by p38 was
dependent on
c-Jun down-regulation
Fuchs-Young et al., Breast Cancer Res Treat 2011
(Cell Transformation, Neoplastic...) :
Previous studies from our laboratory have shown that
p53 regulates ER expression transcriptionally, by binding the ER promoter and forming a complex with CARM1, CBP,
c-Jun , RNA polymerase II and Sp1
Reyes-Zurita et al., BMC cancer 2011
(Colonic Neoplasms) :
We found that in HT29 cells maslinic acid activated the expression of
c-Jun NH2-terminal kinase (JNK) , thus
inducing p53
Chan et al., International journal of molecular sciences 2011
:
In the current study, pretreatment with nitric oxide ( NO ) scavengers inhibited PDT induced mitochondrial membrane potential ( MMP ) changes,
activation of caspase-9, caspase-3, p21 activated protein kinase 2 (PAK2) and
c-Jun N-terminal kinase (JNK) , and gene expression of
p53 and p21 involved in apoptotic signaling
Park et al., Mol Carcinog 2012
(Colonic Neoplasms...) :
HFD feeding increased tumor tissue levels of Ki67, cyclin A, cyclin D1, CDK2, Bcl-xL, and Bcl-2 ; reduced
p53 levels and TUNEL positive apoptotic cells ; increased the levels of CD45, CD68, CD31, VEGF, P-VEGF receptor-2, iNOS, and COX-2 as well as hemoglobin content ; and
increased the levels of HIF-1a, P-STAT3-Y705, P-STAT3-S727, P-I?B-a, P-p65, p65,
P-c-Jun , P-Akt, P-ERK1/2, P-p38, and P-SAPK/JNK
Saha et al., PloS one 2012
(Multiple Myeloma) :
On the other hand,
p53 transcriptional inhibitor, PFT-a or p53 siRNA not only inhibited the activation of p53 transcriptional targets but also
blocked the activation of
c-Jun suggesting the presence of a positive feedback loop between p53 and JNK
Wei et al., Proc Natl Acad Sci U S A 2012
:
Expression of
d133p53 , in response to H. pylori infection, is
regulated by phosphorylation of c-Jun and activation of
activator protein-1 dependent transcription
Xiong et al., Journal of the American Heart Association 2013
:
The activation of p66Shc but not
p53 by Arg-II was
dependent on extracellular signal regulated kinases ( ERKs ) and sequential activation of 40S ribosomal protein S6 kinase 1
(S6K1)-c-Jun N-terminal kinases (JNKs)
Bátor et al., Biochem Cell Biol 2013
:
Cytotoxic concentrations of the nitric oxide donor sodium nitroprusside activated several proapoptotic mechanisms, including stimulation of the stress kinase pathways
mediated by
c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase ( MAPK ), inhibition of the translation initiation factor eIF2a, induction and phosphorylation of the
p53 protein, and inhibited Akt mediated antiapoptotic signaling, independent of Ras function
Casamassimi et al., Cancer Res 1998
:
Fra-1 and c-jun were
induced by
p53 , resulting in increased
AP-1 levels