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CCND1 — 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
Hiyama et al., Cell Death Differ 1999
:
Role for
cyclin D1 in UVC induced and
p53 mediated apoptosis
Liang et al., Virchows Arch 2000
(Bowen's Disease...) :
These findings suggested the hypothesis that prior aberrant
p53 expression may affect or
regulate the overexpression of
cyclin D1
Shao et al., Biochem Biophys Res Commun 2002
(Colorectal Neoplasms) :
p53 inhibits adriamycin induced down-regulation of
cyclin D1 expression in human cancer cells
Pratt et al., J Biol Chem 2003
:
Bcl-2 controls caspase activation following a
p53 dependent
cyclin D1-induced death signal
Rocha et al., Mol Cell Biol 2003
:
p53 represses
cyclin D1 transcription through down regulation of Bcl-3 and inducing increased association of the p52 NF-kappaB subunit with histone deacetylase 1
Guo et al., Mol Cell Biol 2004
:
We found that ( i ) p19(Arf) or p53 deficiency led to a significant increase in PI 3-kinase activity, which in turn upregulated RhoA and Rac1 activities ; ( ii ) deletion of p19Arf or p53 led to an increase in cell growth rate that was in part dependent on RhoA, Rac1, and Cdc42 activities ; ( iii ) p19(Arf) or
p53 deficiency
caused an enhancement of the growth related transcription factor NF-kappa B and
cyclin D1 activities that are partly dependent on RhoA or Cdc42 but not on Rac1 ; ( iv ) forced expression of the activating mutants of Rac1, RhoA, or Cdc42 caused a hyperproliferative phenotype of the p19Arf ( -/- ) and p53 ( -/- ) cells and promoted transformation of both cells ; ( v ) RhoA appeared to contribute to p53 regulated cell proliferation by modulating cell cycle machinery, while hyperactivation of RhoA further suppressed a p53 independent apoptotic signal ; and ( vi ) multiple pathways regulated by RhoA, including that of Rho-kinase, were required for RhoA to fully promote the transformation of p53 ( -/- ) cells
Lu et al., J Cell Physiol 2007
:
We found that the decrease in
cyclin D1 levels induced by NO was GSH-sensitive implying that the redox regulation of NO-mediated cytostasis was a multifaceted process and that both
p53/p21 ( cip1/waf1 ) and p53 independent cyclin D1 pathways were
involved
Chhipa et al., Exp Cell Res 2007
(Breast Neoplasms) :
Therefore this p53 null cell line indicates that
p53 is an indispensable component of cellular signaling system which is regulated by caveolin-1 expression, involving Akt activation and
increase in
cyclin D1 , thereby promoting proliferation of breast cancer cells
Guo et al., Biochim Biophys Acta 2009
:
Importantly,
p53 overexpression can
prevent cyclin D1 promoter activation by p65
Ray et al., Cancer Res 2010
(Breast Neoplasms) :
Further studies revealed that BME treatment enhanced
p53 , p21, and pChk1/2 and
inhibited cyclin B1 and
cyclin D1 expression, suggesting an additional mechanism involving cell cycle regulation
Gatouillat et al., J Cell Biochem 2010
(Melanoma, Experimental) :
This was accomplished by imposing an artificial checkpoint at the G ( 1 ) -S phase transition, as demonstrated by cell-cycle analysis and down-regulation of
cyclin D1/cdk4 and
increased of
p53 expression level
Lee et al., J Cell Biochem 2011
:
In the cell cycle related proteins, SJSZ glycoprotein ( 50 ?µg/ml ) significantly
enhances the expression of
p53 , p21, and p27, whereas it suppressed the activity of
cyclin D1/CDK4
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
Brennan et al., J Med Food 2012
(Adrenocortical Carcinoma) :
BME treatment enhanced cellular tumor antigen
p53 , cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and
inhibited G1/S-specific cyclin D1 , D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival
Abdelalim et al., Biochem Biophys Res Commun 2012
:
In addition, inhibition of
p53 activity
reduced the expression levels of
cyclin D1 and Nanog
Liu et al., PloS one 2012
(Stomach Neoplasms) :
In addition, the expression level of p21,
p53 and Caspase-9 were increased when AP-4 was knockdown, but the expression of
cyclin D1 , Bcl-2 and Bcl-x ( L ) was
inhibited
Chen et al., Cancer Res 1995
:
p53 , through p21 ( WAF1/CIP1 ),
induces cyclin D1 synthesis ... We show here that accumulation of the wild-type
p53 protein in either human or murine cells markedly
increases expression of
cyclin D1
Spitkovsky et al., Oncogene 1995
:
The
role of
p53 in coordinated regulation of
cyclin D1 and p21 gene expression by the adenovirus E1A and E1B oncogenes ... Since E1B was shown to target p53, we investigated the
role of
p53 for expression of the
cyclin D1 gene