Gene interactions and pathways from curated databases and text-mining

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PCNA — 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

Kato et al., Leukemia & lymphoma 1999 (Leukemia, Erythroblastic, Acute) : In this process, p53 recovered the wild-type p53 function and the expression of the p21 ( waf1/cip1/sdi1 ), cyclin G1 and gadd45 genes was increased
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
Chang et al., J Cell Biochem 1999 : In addition, the role of p53 in the UV induction of rat PCNA promoter was investigated ... Therefore, it is unlikely that the UV induction of the rat PCNA promoter is p53 dependent
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
Tut et al., Br J Cancer 2001 (Carcinoma, Transitional Cell...) : Cyclin/cdk complexes are generally inhibited by cyclin dependent kinase inhibitors(ckis) , some of which are induced by wild-type p53
Paunesku et al., Int J Radiat Biol 2001 : The PCNA gene is induced by p53 , while PCNA protein interacts with p53 controlled proteins Gadd45, MyD118, CR6 and, most importantly, p21, in the process of deciding cell fate
Saifudeen et al., American journal of physiology. Renal physiology 2002 : Spatial repression of PCNA by p53 during kidney development ... Because p53 induced growth arrest correlates with downregulation of PCNA gene expression, we examined the impact of p53 inactivation on PCNA expression in mice and evaluated the effect of p53 on PCNA transcription ... Interestingly, deletion of the p53 binding site confers enhanced responsiveness to p53 mediated repression, suggesting that transcriptional repression of PCNA by p53 is achieved by a mechanism other than direct DNA binding
Bossenmeyer-PouriƩ et al., Neuroscience 2002 (Hypoxia, Brain) : Transient overexpression of proliferating cell nuclear antigen was followed by increasing expression of p53 , p21, Bax and caspases, whereas Bcl-2 and heat shock proteins were progressively repressed
Chang et al., Ann N Y Acad Sci 2002 : The roles of p53 , DNA repair, and oxidative stress in ultraviolet C induction of proliferating cell nuclear antigen expression
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
Ohtsuka et al., Oncogene 2003 : Cyclin G expression resulted in a dramatic decrease of p53 protein levels in response to DNA damage and abrogated irradiation mediated G1 arrest along with an increase of S phase in MCF7 cells containing wild-type p53
Cabello et al., J Submicrosc Cytol Pathol 2003 (Adenocarcinoma...) : These results showed that parathion and malathion increased PCNA and induced mutant p53 protein expression of MCF7 cells in comparison to controls and atropine inhibited such action
Li et al., Breast Cancer Res Treat 2003 (Breast Neoplasms) : We show that the expression of p21 was upregulated and expressions of cdc2, cyclin B2 and protein regulator of cytokinesis 1 ( PRC1 ) were suppressed by overexpression of the wt p53 in MCF7-ptsp53 cells at the permissive temperature
Shan et al., J Biol Chem 2003 : Induction of p53 dependent activation of the human proliferating cell nuclear antigen gene in chromatin by ionizing radiation
Subler et al., J Virol 1992 : We studied the effects of wild-type and mutant human p53 on the human proliferating-cell nuclear antigen promoter and on several viral promoters including the simian virus 40 early promoter-enhancer, the herpes simplex virus type 1 thymidine kinase and UL9 promoters, the human cytomegalovirus major immediate-early promoter-enhancer, and the long terminal repeat promoters of Rous sarcoma virus, human immunodeficiency virus type 1, and human T-cell lymphotropic virus type I. HeLa cells were cotransfected with a wild-type or mutant p53 expression vector and plasmids containing a chloramphenicol acetyltransferase reporter gene under viral ( or cellular ) promoter control
Deb et al., J Virol 1992 : We, therefore, have studied the effects of wild-type and mutant human p53 on the human proliferating-cell nuclear antigen ( PCNA ) promoter and on several viral promoters, including the herpes simplex virus type 1 UL9 promoter, the human cytomegalovirus major immediate-early promoter-enhancer, and the long terminal repeat promoters of Rous sarcoma virus and human T-cell lymphotropic virus type I. HeLa cells were cotransfected with a wild-type or mutant p53 expression vector and a plasmid containing a chloramphenicol acetyltransferase reporter gene under viral ( or cellular ) promoter control ... The activation of PCNA by mutant p53s may indicate a way to increase cell proliferation by the mutant p53s
Kemp et al., J Nutr 2003 (Breast Neoplasms...) : In contrast, the overexpression of mutant p53 ( 175Arg to His ) in MFC-7 cells prevented the CLA dependent accumulation of p21 and the reduction of cyclin E levels suggesting that the expression of wild-type p53 is required for CLA mediated activation of the G1 restriction point
Ghatnekar et al., Birth Defects Res A Clin Mol Teratol 2004 (Hypoglycemia) : Protein expression of caspase-3 active subunit and p53 was increased and PCNA was markedly reduced in hearts of embryos exposed to hypoglycemia
Ohtsuka et al., Oncogene 2004 : However, cyclin G does not cause similar reductions in p53 levels in ATM mutated cells
Yu et al., J Alzheimers Dis 2005 (Neuroblastoma) : Pretreatment of cells with cdk inhibitor olomoucine impeded cdk2-cyclin E accumulation, but not the induction of p53
Chang et al., J Virol 2008 : We showed that the ectopic expression of K-cyclin led to a sustained increase of p53 phosphorylation on Ser ( 33 ) in vivo, and the phosphorylation could be inhibited by a dominant negative Cdk9 mutant, dn-Cdk9
Levesque et al., Mol Cancer Ther 2008 (Neoplasms) : Defective p53 signaling in p53 wild-type tumors attenuates p21waf1 induction and cyclin B repression rendering them sensitive to Chk1 inhibitors that abrogate DNA damage induced S and G2 arrest
Bosque et al., J Leukoc Biol 2008 (Autoimmune Diseases...) : Our data indicate that in human CD8+ T-cell blasts, Fas ligation, and especially Apo2L/TRAIL induce the p53 dependent decrease in cyclin-B1 levels
Shen et al., Cancer Res 2008 (Neoplasms...) : p53-p21 pathway activation was required for the depletion of Cyclin B1, Cyclin A, and CDC2 in Nutlin-3a treated cells and for endoreduplication after Nutlin-3a removal
Toettcher et al., Proc Natl Acad Sci U S A 2009 : We find that different arrest mechanisms serve indispensable roles in the proper cellular response to DNA damage over time : p53 independent cyclin inactivation confers immediate arrest, whereas p53 dependent cyclin downregulation allows this arrest to be sustained
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 )
Liu et al., BMC cancer 2010 (Brain Neoplasms...) : Changes in several cell cycle regulators such as Cyclins D1 and E, PCNA and Ki67, and several apoptosis related regulators such as p53 , p-JNK, p-AKT, and PARP were determined by Western blot analysis
Pang et al., Zhongguo Fei Ai Za Zhi 2003 : Cisplatin could obviously inhibit the proliferation of the cells, and IC50 value for cisplatin treatment was 18.47 mg/L. Cisplatin could obviously down-regulate telomerase activity, decrease S phase cells, increase G0/G1 phase cells, decline the expressions of bcl-2 and PCNA proteins and induce the expression of p53 protein of SLC-89 cells in a concentration dependent fashion
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
Ummanni et al., Molecular cancer 2011 (Prostatic Neoplasms) : In further analysis, we found evidence that exogenous expression of UCHL1 suppress LNCaP cells growth probably via p53 mediated inhibition of Akt/PKB phosphorylation and also via accumulation of p27kip1 a cyclin dependant kinase inhibitor of cell cycle regulating proteins
Harper et al., Mol Biol Cell 1995 : p21Cip1 is a cyclin dependent kinase (Cdk) inhibitor that is transcriptionally activated by p53 in response to DNA damage
Yamaguchi et al., Eur J Biochem 1994 (Neuroblastoma) : Analysis with various deletion mutants in the PCNA gene promoter revealed that a specific sequence is not required for the repression, suggesting that p53 represses the PCNA gene promoter by interacting with some components of the basic transcription machinery
Jackson et al., Biochem Biophys Res Commun 1994 : Transcriptional regulation of the PCNA promoter by p53 ... In HeLa cells, p53 activates the PCNA promoter whereas in CV1, CHO, L929, and Saos-2 cells the same promoter is strongly repressed
Yamamoto et al., Exp Cell Res 1994 : Our data support the idea that tumor suppressors modulate the expression of cell cycle-regulatory genes : RB regulates p34cdc2 expression and p53 regulates cyclin A expression
Shivakumar et al., Mol Cell Biol 1995 : Wild-type human p53 transactivates the human proliferating cell nuclear antigen promoter ... Here, using a number of different cell lines and transient-transfection-transcription assays, we demonstrate that at low levels, wild-type p53 transactivates the human proliferating cell nuclear antigen ( PCNA ) promoter ... When expressed at a similar level, the tumor derived p53 mutants did not transactivate the PCNA promoter ... Deletion of the p53 binding site renders the PCNA promoter p53 nonresponsive, showing that wild-type p53 transactivates the PCNA promoter by binding to the site ... At a higher concentration, wild-type p53 inhibits the PCNA promoter but p53 mutants activate ... These observations suggest that moderate elevation of the cellular wild-type p53 level induces PCNA production to help in DNA repair
Morris et al., Proc Natl Acad Sci U S A 1996 (Li-Fraumeni Syndrome) : Transcriptional activation of the human proliferating-cell nuclear antigen promoter by p53 ... Activation of the PCNA promoter by wild-type p53 depends upon the level of p53 expression ... This concentration dependence and cell type specificity reconciles the observations presented here with prior results indicating that wild-type p53 represses the PCNA promoter
Vikhanskaya et al., Exp Cell Res 1996 (Ovarian Neoplasms) : Treatment with DX or AMSA caused similar effects, suggesting that p53 induced changes in cyclin , cdk, and cdk inhibitors after DNA damage are not responsible for the marked reduction in the cytotoxicity of DX we observed in wt p53 expressing cells
Inohara et al., Br J Dermatol 1996 (Carcinoma, Squamous Cell...) : p21Waf1/Cip1 is a cyclin dependent kinase (CDK) inhibitor induced by wild-type p53
Buckley et al., Am J Physiol 1997 : Herein, we have determined that, in adult rat AEC2 in primary culture on Engelbreth-Holm-Swarm biomatrix ( Matrigel ) in the presence of keratinocyte growth factor, the expression of key cell cycle control elements, including cyclins A and D and cyclin dependent kinases (cdk) 1 and 4, is increased and that retinoblastoma protein ( pRb ) phosphorylation is also increased , with a corresponding decrease in the expression of p53 and the cdk inhibitors ( cdkis ) p21WAF1/CIP1 and p27KIP-1 compared with cells cultured on plastic
Xie et al., Oncogene 1998 (Ataxia Telangiectasia) : We investigated the requirements for protein p53 and the ATM gene product in radiation induced inhibition of DNA synthesis and regulation of the cyclin E/ and cyclin A/cyclin dependent kinases (Cdks)
Karuppayil et al., J Biol Chem 1998 : Our results showed that whereas both p53 and 12 S E1A separately activated PCNA transcription, 12 S E1A repressed p53 mediated transcriptional activation
Li et al., Cancer Res 1998 (Leukemia, Myeloid, Acute) : p53 and p21/Cip1, respectively, inhibit the expression and activation of PCNA , whereas p130 and pRb, respectively, inhibit the expression and activation of E2F1
Xu et al., Mol Cell Biol 1999 : p53 mediated regulation of proliferating cell nuclear antigen expression in cells exposed to ionizing radiation ... These findings suggest a complex cellular response to DNA damage in which p53 transiently activates expression of PCNA for the purpose of limited DNA repair