Gene interactions and pathways from curated databases and text-mining

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CCNG1 — TP53

Pathways - manually collected, often from reviews:

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
Verdoodt et al., Mutagenesis 1999 (Leukemia...) : The results in KS, as compared with K562, confirm that wild-type p53 can prevent further cycling of polyploid cells by blocking rereplication
Yoon et al., Exp Hematol 2001 : The likelihood that suppression of bone marrow cellularity and cell cycling is mediated by p53 was supported by the upregulation of p21, a cyclin dependent kinase inhibitor
Galmarini et al., Br J Cancer 2001 : MN1 cells, but not MDD2 cells, displayed wt-p53 protein accumulation as well as p21/WAF1 and cyclin G1 induction after exposure to TBA
Kimura et al., Genes Cells 2002 : Cyclin G1 associates with MDM2 and regulates accumulation and degradation of p53 protein
Jensen et al., Hepatology 2003 (Liver Neoplasms) : Recent data show that cyclin G1 can regulate the levels of p53 by a mechanism that involves dephosphorylation of Mdm2 by protein phosphatase 2A
Ohtsuka et al., Oncogene 2004 : However, cyclin G does not cause similar reductions in p53 levels in ATM mutated cells
Yew et al., Nature 1992 (Cell Transformation, Viral) : These results indicate that p53 probably inhibits cell cycling by functioning as a transcription factor
Tsuchihara et al., Cancer Res 2005 (Aneuploidy...) : Ckap2 regulates aneuploidy, cell cycling , and cell death in a p53 dependent manner
Braithwaite et al., Virology 1990 : Experiments with hydroxyurea show that p53 activation does not require continued cell cycling and thus is likely to be a direct consequence of viral gene expression
Wang et al., Hepatology 2012 (Colorectal Neoplasms...) : Using coimmunoprecipitation, a luciferase reporter system, and electrophoretic mobility shift assay, we further demonstrated that cyclin G(1) specifically interacted with p53, and this interaction blocked the specific binding of p53 to HBV enhancer elements and simultaneously abrogated p53 mediated inhibition of HBV transcription
Apostolidis et al., Physiol Genomics 2012 : In primary megakaryocytes and in the megakaryocytic cell line CHRF, loss or knock-down of p53 enhances cell cycling and inhibits apoptosis, leading to increased polyploidization
Colombel et al., Oncogene 1995 : However, wild-type p53 does appear to enhance this process, especially in the early period following castration, and this protein may regulate an aberrant prostate cell cycling activity that follows castration
Elias et al., Int J Dermatol 1995 (Psoriasis) : Since PCNA is a marker of cellular proliferation and p53 inhibits cellular cycling , some of the beneficial effects of PTU and MMI in psoriasis may depend on the ability of the drugs to impair cellular turnover, perhaps by binding to the triiodothyronine ( T3 ) receptor
Bates et al., Oncogene 1996 : Both human G-cyclins are induced by the DNA damaging agent actinomycin-D and although the induction of cyclin G1 is clearly p53 dependent , activation of cyclin G2 expression was observed in the absence of p53
Shimizu et al., Biochem Biophys Res Commun 1998 : To investigate regulation mechanisms of G2/M phase transition, we studied the association of cell cycle progression with p53 dependent p21/waf-1 and cyclinG expression
Jensen et al., Hepatology 1998 : The expression of cyclin G1 is induced by transforming growth factor beta1 and p53 , as well as by multiple mitogenic stimuli in mammalian cells in culture