◀ Back to TP53
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