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RAD51 — TP53

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: RAD51 — TP53 (physical association, affinity chromatography technology) Dong et al., Mol Cell 2003
• IRef Biogrid Interaction: RAD51 — TP53 (association, biochemical) Dong et al., Mol Cell 2003
• IRef Biogrid Interaction: RAD51 — TP53 (direct interaction, pull down) Buchhop et al., Nucleic Acids Res 1997*
• IRef Biogrid Interaction: RAD51 — TP53 (direct interaction, pull down) Stürzbecher et al., EMBO J 1996*
• IRef Biogrid Interaction: RAD51 — TP53 (physical association, affinity chromatography technology) Stürzbecher et al., EMBO J 1996*
• IRef Biogrid Interaction: RAD51 — TP53 (physical association, affinity chromatography technology) Nakai-Murakami et al., Oncogene 2007*
• IRef Biogrid Interaction: RAD51 — TP53 (physical association, affinity chromatography technology) Yang et al., Oncogene 2004*
• MIPS CORUM MSH2/6-BLM-p53-RAD51 complex: MSH2/6-BLM-p53-RAD51 complex complex (BLM-MSH2-MSH6-RAD51-TP53) Yang et al., Oncogene 2004*
• IRef Corum Interaction: Complex of 11 proteins (association, anti bait coimmunoprecipitation) Yang et al., Oncogene 2004*
• IRef Hprd Interaction: TP53 — RAD51 (in vivo) Marmorstein et al., Proc Natl Acad Sci U S A 1998*
• IRef Hprd Interaction: Complex of 17 proteins (in vivo) Yang et al., Oncogene 2004*
• IRef Hprd Interaction: TP53 — RAD51 (in vitro) Stürzbecher et al., EMBO J 1996*, Buchhop et al., Nucleic Acids Res 1997*
• IRef Hprd Interaction: TP53 — RAD51 (in vivo) Stürzbecher et al., EMBO J 1996*, Buchhop et al., Nucleic Acids Res 1997*
• IRef Intact Interaction: RAD51 — TP53 (physical association, coimmunoprecipitation) Buchhop et al., Nucleic Acids Res 1997*
• IRef Ophid Interaction: RAD51 — TP53 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Magnusson et al., Gene 2000 (Bloom Syndrome) : The lack of sufficient levels of wild-type p53 and increased levels of HsRad51 protein may contribute to the elevated RecA-like activity in the GM1492 fibroblasts
Tang et al., J Biol Chem 2002 : In response to DNA damage, ataxia-telangiectasia mutant and ataxia-telangiectasia and Rad-3 activate p53 , resulting in either cell cycle arrest or apoptosis
Kumari et al., Oncogene 2004 : Altogether, we suggest that the effect of p53 on HR and RAD51 levels and foci can be explained by the idea that p53 suppresses formation of recombinogenic lesions
Arias-Lopez et al., EMBO Rep 2006 : We propose that transcriptional repression of Rad51 by p53 participates in regulating homologous recombination, and impaired Rad51 repression by p53 mutants may contribute to malignant transformation
Lazaro-Trueba et al., Cell cycle (Georgetown, Tex.) 2006 (Cell Transformation, Neoplastic) : The regulation of homologous recombination ( HR ) by p53 has been currently associated with its nontransactivating function ; now the transcriptional repression of the Rad51 gene by p53 has been elucidated
Ambrosini et al., Cancer Res 2008 (Colonic Neoplasms) : The cyclin dependent kinase inhibitor flavopiridol potentiates the effects of topoisomerase I poisons by suppressing Rad51 expression in a p53 dependent manner ... Microarray analysis also revealed suppression of Rad51 in a p53 dependent manner ... In conclusion, after DNA damage by Topo I poisons, flavopiridol targets homologous recombination through a p53 dependent down-regulation of Rad51 , resulting in enhancement of apoptosis
Schild et al., Nucleic Acids Res 2010 (Genomic Instability...) : Of particular interest, this model may also help explain the high frequency of TP53 mutations in human cancers, since wild-type p53 represses RAD51 expression
Nottke et al., Proc Natl Acad Sci U S A 2011 : SPR-5 shows enzymatic activity toward H3K4me2 both in vitro and in the nematode germline, and spr-5 mutants show several phenotypes indicating a perturbation of DSBR, including increased p53 dependent germ cell apoptosis, increased levels of the DSBR marker RAD-51 , and sensitivity toward DSB inducing treatments
Liu et al., Anticancer Res 2011 (Breast Neoplasms) : The p53 pathway was involved in the synergism of RAD001 and carboplatin on breast cancer cell proliferation and apoptosis, since the synergistic effect was demonstrated in all tested breast cancer cell lines with wild-type p53 and the use of p53 inhibitor partially antagonized the effect of RAD001 and carboplatin on p53 and p21 expression, as well as their inhibitory effect on cell proliferation
Fong et al., PloS one 2011 (Neoplasms) : Exogenous expression of p53 in a p53 null cell line strongly suppressed activity of the Rad51 core promoter, underscoring the selectivity of this promoter for p53-deficient cells
Ghosh et al., J Radiat Res 2012 (Neutropenia...) : The results demonstrated that Ex-RAD ameliorates radiation induced peripheral blood cell depletion, promotes bone marrow recovery, reduces p53 signaling in spleen and protects intestine from radiation injury
Buchhop et al., Nucleic Acids Res 1997 : These data are consistent with the hypothesis that p53 interaction with hRAD51 may influence DNA recombination and repair and that additional modifications of p53 by mutation and protein binding may affect this interaction