Gene interactions and pathways from curated databases and text-mining

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CCNB1 — TP53

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Taylor et al., Mol Biol Cell 1999 : Transcription of cdc2 and cyclin B1 , determined using reporter constructs driven by the two promoters, was suppressed in response to the induction of p53
Park et al., Cancer Res 2000 : Biochemical analysis showed that p53 inhibits cell cycle dependent expression of cdc2 and cyclin B1 and consequently inhibits cdc2 kinase
Taylor et al., J Biol Chem 2001 : p53 represses the transcription of cdc2 and cyclin B1 , causing loss of Cdc2 activity and G ( 2 ) arrest
Krause et al., Nucleic Acids Res 2000 : Taken together with earlier observations on p53 dependent transcription of cyclin B1 , our results suggest that one way of regulating G ( 2 ) arrest may be a reduction in cyclin B levels through p53 dependent transcriptional repression
Dan et al., Biochem Biophys Res Commun 2001 (Lung Neoplasms) : Previous reports have shown that overexpression of p53 represses cyclin B1 transcription
Taylor et al., Oncogene 2001 : Binding of Cdc2 to Cyclin B1 is required for its activity, and repression of the cyclin B1 gene by p53 also contributes to blocking entry into mitosis
Yin et al., Cancer Res 2001 : Inverse regulation of cyclin B1 by c-Myc and p53 and induction of tetraploidy by cyclin B1 overexpression
Li et al., Radiat Res 2002 : The level of cyclin B1 , required for CDC2 activity, was decreased in the presence of functional TP53
Yu et al., Mol Immunol 2002 (Neoplasms) : We conclude that p53 plays an important role in cyclin B1 regulation and that tumors with mutated p53 will be good candidates for cyclin B1 based immunotherapy
Clifford et al., Cancer Res 2003 (Fibrosarcoma) : We have previously found that the overexpression of p53 causes G ( 2 ) arrest and represses the synthesis of cyclin dependent kinase 1 and cyclin B1 , two proteins required for cells to traverse from G ( 2 ) into M. G ( 2 ) arrest occurs in response to DNA damage caused by a variety of agents and treatments
Innocente et al., Biochem Biophys Res Commun 2005 : We have previously reported that p53 prevents G ( 2 ) /M transition by decreasing intracellular levels of both cyclin B1 mRNA and protein, and attenuating the activity of the cyclin B1 promoter
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
Nantajit et al., PloS one 2010 : Herein, we reveal an anti-apoptotic role of mitochondrial p53 regulated by the cell cycle complex cyclin B1/Cdk1 in irradiated human colon cancer HCT116 cells with p53 ( +/+ ) status