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CDKN1A — JUN
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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
Kardassis et al., J Biol Chem 1999
:
In the present study we show that the Sp1 occupied promoter region mediates
transactivation of the
p21 promoter by
c-Jun and the related proteins JunB, JunD, and ATF-2 ... By utilizing the same assay, we found that the glutamine-rich segment of the B domain of Sp1 ( Bc, amino acids 424-542 ) was sufficient for
c-Jun induced transactivation of the
p21 promoter
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
Perlman et al., J Immunol 2003
(Arthritis, Rheumatoid) :
Furthermore, in RA synovial fibroblasts the ectopic expression of
p21 reduces activation of the
AP-1 transcription factor
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
Kolomeichuk et al., Mol Pharmacol 2008
:
In KB-3 cells, which have compromised p53 function, and in p53-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression concomitant with increased c-Jun expression, suggesting a
role for
c-Jun in negative regulation of the
p21 promoter independent of p53
Chan et al., IUBMB Life 2008
:
Experiments with the embryonic stem cell line, ESC-B5, disclose that CTN induces apoptosis via several mechanisms, including ROS generation, increased cytoplasmic free calcium levels, intracellular nitric oxide production, enhanced Bax/Bcl-2 ratio, loss of mitochondrial membrane potential, cytochrome c release, activation of caspase-9 and caspase-3, and
p21 activated protein kinase 2 and
c-Jun N-terminal protein kinase activation
Lotan et al., Cancer Res 2008
(Neoplasm Metastasis...) :
c-Jun NH2-terminal kinase activating kinase 1/mitogen activated protein kinase kinase 4-mediated inhibition of SKOV3ip.1 ovarian cancer metastasis
involves growth arrest and
p21 up-regulation
He et al., J Biochem 2009
(MAP Kinase Signaling System) :
Here, we show that Ang II upregulated KLF5 and
c-Jun expression and
inhibited p21 expression in VSMCs, and silencing of KLF5 expression by KLF5-specific small interfering RNA ( siRNA ) neutralized the inhibitory effects of Ang II on p21 expression
Hsu et al., J Cell Biochem 2009
(Neovascularization, Pathologic) :
The aim of this study is to examine the
involvement of
c-Jun NH2-terminal kinase (JNK) in the TB-induced increase of
p21 protein level and DNA synthesis inhibition
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