Gene interactions and pathways from curated databases and text-mining

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CDK2 — TP53

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Ariazi et al., Cancer Res 1999 (Mammary Neoplasms, Animal) : RNA expression studies, based on a multiplexed-nuclease protection assay, demonstrated that cell cycle- and apoptosis related genes were differentially expressed within 48 h of POH treatment ; p21 ( Cip1/WAF1 ), bax, bad, and annexin I were induced ; cyclin E and cyclin dependent kinase 2 were repressed ; and bcl-2 and p53 were unchanged
Shackelford et al., Environ Health Perspect 1999 (Ataxia Telangiectasia...) : These responses include the p53 dependent and p53 independent induction of Cdk inhibitors and the p53 independent inhibitory phosphorylation of Cdk molecules themselves
Kourea et al., Am J Pathol 1999 (Cell Transformation, Neoplastic...) : In this study, we investigated patterns of expression of p53 and pRB, cyclin dependent kinase inhibitors ( CKIs ) p21 and p27, as well as cyclins D1 and E, in a cohort of 35 well characterized MPNSTs and 16 NFs
David-Pfeuty et al., Oncogene 1999 (Breast Neoplasms...) : At concentrations equal or superior to respectively 30- and 20-fold their in vitro IC50 values for cyclin B/Cdk1, cyclin A/Cdk2 and cyclin E/Cdk2, the Cdk inhibitors precipitately induce a dramatic nuclear accumulation of wt p53 and a delocalization of nucleolin from the nucleolus in all interphase cells, whatever their cell cycle status, acting in this way like the DNA damaging drug, mitomycin C ( 7 microg/ml )
Woodward et al., Anticancer Res 2000 (Barrett Esophagus...) : P21 is a cyclin dependent kinase inhibitor that is activated by p53
Morris et al., J Neurosci 2001 : An increase in p53 protein levels, nuclear localization, and DNA binding that result from DNA damage are not affected by the inhibition of CDK activity ... However, either p53 deficiency or the inhibition of CDK activity alone inhibited Bax translocation, cytochrome c release, and caspase-3-like activation
Jaiswal et al., Int J Oncol 2001 (Colonic Neoplasms) : However, with cyclin dependent kinase ( Cdk2 ) and TFIIH complex associated kinase CAK, the phosphorylation of p53 was increased at later time points ( 25 h )
Arnould et al., EMBO J 2002 : Finally, our data suggest that phosphorylated CREB recruits p53 tumor suppressor protein, modifies its transcriptional activity and increases the expression of p21 ( Waf1/Cip1 ), a p53 regulated cyclin dependent kinase inhibitor
Wunderlich et al., Oncogene 2002 : Taken together, these results suggest that Mdm2 activation of E2F1 occurs through the repression of p53 dependent transcription of p21, a p53-target gene and cyclin dependent kinase inhibitor
Tang et al., J Clin Endocrinol Metab 2002 (Ovarian Neoplasms) : The protein levels of p21 ( a Cdk inhibitor ) and p53 ( a suppressor of tumor cell growth and a positive regulator for p21 expression ) were increased by Cetrorelix, but the levels of p27 ( a Cdk inhibitor ) did not change significantly
Yamasaki et al., Cancer Treat Res 2003 (Neoplasms) : Following DNA damage, the p53 dependent induction of p21CIP1 regulates cyclin E/Cdk2 and cyclin A/Cdk2 complexes both of which phosphorylate pRB, leading to E2F mediated activation
Wyllie et al., Exp Cell Res 2003 : Mutant p53 can delay growth arrest and loss of CDK2 activity in senescing human fibroblasts without reducing p21 ( WAF1 ) expression
Xie et al., J Biol Chem 2003 : For comparison, the tumor suppressor p53 represses CDK2 promoter activity independently of IRF1 through sequences upstream of nt -68, and the CDP/cut/Cux1 homeodomain protein represses transcription down-stream of -31
Hill et al., J Cell Biochem 2004 : We report that expression of dominant negative SWI/SNF enzymes does not affect p53 mediated induction of the p21 cyclin dependent kinase inhibitor or the Mdm2 E3 ubiquitin ligase that regulates p53 in cells exposed to UV or gamma irradiation
Lum et al., J Cutan Pathol 2004 (Carcinoma, Basal Cell...) : The other p53 dependent, cyclin dependent kinase inhibitor , p27(kip-1), has shown to be increased in TEps, which is consistent with this benign neoplasm 's better differentiated state
He et al., Oncogene 2005 : Induction of p21 by p53 following DNA damage inhibits both Cdk4 and Cdk2 activities ... Although there is ample evidence that p21 induction by p53 leads to Cdk2 inhibition, it is unclear whether this checkpoint event also leads to Cdk4 inhibition ... Together, these findings establish that activation of the p53-p21 pathway is responsible for the DAP induced G ( 1 ) -phase checkpoint response and provide the first solid evidence that p21 induction by p53 during a DNA damage induced G ( 1 ) -phase checkpoint response inhibits both Cdk4 and Cdk2 activities
Chia et al., Ann N Y Acad Sci 2005 (Glioma) : In conclusion, these data suggest that thallium acetate inhibits cell cycle progression at G2/M phase by suppressing CDK activity through the p53 mediated induction of the CDK inhibitor p21(Cip1)
Wesierska-Gadek et al., Expert Opin Investig Drugs 2006 (Neoplasms) : Interestingly, some CDK inhibitors additionally affect the stability and activity of the tumour-suppressor protein p53 , thereby enhancing their antiproliferative action towards cancer cells
Voorhoeve et al., Cell 2006 (Neoplasms, Germ Cell and Embryonal...) : These miRNAs neutralize p53 mediated CDK inhibition, possibly through direct inhibition of the expression of the tumor-suppressor LATS2
Payton et al., Cancer Res 2006 (Neoplasms) : Although CDK inhibitors activate p53 , the inhibitors were equipotent in arresting the cell cycle in isogenic breast and colon tumor cells lacking p53, suggesting the response is independent of p53
Voorhoeve et al., Adv Exp Med Biol 2007 (Cell Transformation, Neoplastic...) : These miRNAs neutralize p53 mediated CDK inhibition, possibly through direct inhibition of the expression of the tumorsuppressor LATS2
Zhao et al., Toxicology 2008 (Adenocarcinoma...) : Our results indicate that MnCl2 orderly induces G0/G1 and S phase arrest in A549 cells, the decreasing of Cdk4, Cdk2 and Cyclin A, and the increasing of p53 and Cdks inhibitor WAF1/p21 might be responsible for the G0/G1 arrest, and the decreasing of Cdk4 and Cdk2 levels for the S phase arrest
Zhang et al., J Biol Chem 2008 : Thus, CDK inhibitors suppress MDM2 levels and enhance p53 expression that facilitates bile acid induced, ceramide dependent CD95 activation to induce both apoptosis and autophagy in primary hepatocytes
Jung et al., Cell cycle (Georgetown, Tex.) 2009 (Neoplasms) : The p21 gene encodes a CDK-inhibitor , which is induced by p53 and many other anti-proliferative factors
Kwon et al., Cancer Lett 2010 (Adenocarcinoma...) : Induction of G1 arrest by widdrol was correlated with induction of Chk2, p53 phosphorylation and CDK inhibitor p21 expression as well as inhibition of cyclin E, cyclin dependent kinase ( CDK2 ) and retinoblastoma protein ( pRB )
Muth et al., Cancer Res 2010 (Neuroblastoma) : In contrast, doxorubicin or nutlin-3 treatment-both leading to p53-p21 activation-or CDK2 inhibition had no effect on SKP2 regulation in MYCN amplified cells
Takahashi et al., Int J Oncol 1994 : The present results suggest that the nuclear exclusion and complex formation of p53 with p44 in the cytoplasm control DNA synthesis by reducing p21 expression, thereby leading to the activation of CDK2
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
Chew et al., J Biol Chem 2012 : Sulforaphane induction of p21 ( Cip1 ) cyclin dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53 dependent
Soares et al., Ecotoxicology 2012 : Real time PCR was used to analyse the expression levels of nucleotide excision repair genes ( NER ) as well as the tumor suppressor p53 and downstream selected effectors, i.e., p21 ( cyclin dependent kinase inhibitor ), GADD45a ( growth arrest and DNA damage induced 45, alpha ), bax ( bcl2 associated X protein ) and p53 key regulator MDM2 ( murine double minute 2 protein )
Du et al., PloS one 2013 (Ovarian Neoplasms) : The present studies demonstrate for the first time that SB225002 has dual actions in OVCA cells, inducing classic apoptosis through p53 activation and provoking mitotic catastrophe in both p53 wild-type and deficient cells by Chk1 inhibition and Cdk activation
Katayose et al., Biochem Biophys Res Commun 1995 : p53 shows its tumor suppresser activity by inducing cell cycle arrest and/or apoptosis of tumor cells and these activities are in part mediated by p21 cyclin dependent kinase inhibitor ( also called as WAF1, Cip1 and SDI1 )
DiGiuseppe et al., Am J Pathol 1995 (Adenocarcinoma...) : The cyclin dependent kinase inhibitor, p21 ( also known as WAF1 and CIP1 ), is induced by wild-type but not mutant p53 , and recent work has implicated p21 as a downstream mediator of the growth suppressing and apoptosis promoting functions of wild-type p53
Deng et al., Cell 1995 (Neoplasms, Experimental) : p21CIP1/WAF1 is a CDK inhibitor regulated by the tumor suppressor p53 and is hypothesized to mediate G1 arrest
Flores-Rozas et al., Proc Natl Acad Sci U S A 1994 : Cdk interacting protein 1 (Cip1) is a p53 regulated 21-kDa protein that inhibits several members of the cyclin dependent kinase (CDK) family
Dulić et al., Cell 1994 : p53 dependent inhibition of cyclin dependent kinase activities in human fibroblasts during radiation induced G1 arrest ... Our data suggest a model in which ionizing radiation confers G1 arrest via the p53 mediated induction of a Cdk inhibitor protein
Khan et al., Carcinogenesis 1997 : In concert with the absence of a G1 arrest, it was found that though both chemical treatments led to increased levels of p53, only the p53 induced by actinomycin D was transcriptionally active and increased the levels of the cyclin dependent kinase inhibitor, p21 ( waf1/cip1 )
Xie et al., Oncogene 1998 (Ataxia Telangiectasia) : The results indicate that neither p53 nor p21 is required for transient inhibition of cyclin E/Cdk2 associated with the G1/S checkpoint or for inhibition of DNA synthesis at ` checkpoints ' within the S phase
Joshi et al., Cancer Gene Ther 1998 (Carcinoma, Non-Small-Cell Lung...) : p21WAF1 ( p21 ) is a cyclin dependent kinase inhibitor that is induced by p53 upon DNA damage or p53 overexpression, resulting in cell cycle arrest at the G1 checkpoint and inhibition of further cell proliferation
Gervais et al., J Biol Chem 1998 : The G1 cell cycle arrest is in part caused by the p53 dependent transcriptional activation of the CDK inhibitor, p21 ( Cip1/Waf1 )
Kelley et al., Oncogene 1998 (Disease Progression...) : However, we detected induction of the p21Cip1 cyclin dependent kinase inhibitor gene during differentiation, which was markedly enhanced in the presence of p53
Gil-Gómez et al., EMBO J 1998 : We found that Cdk2 activation during thymocyte apoptosis can be regulated by p53 , Bax and Bcl-2