Gene interactions and pathways from curated databases and text-mining

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BRCA1 — 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

Somasundaram et al., Oncogene 1999 : BRCA1 does not stabilize p53 in p14ARF-deficient cells
MacLachlan et al., J Biol Chem 2000 : Repression of BRCA1 through a feedback loop involving p53 ... In this study, we show that BRCA1 is initially up-regulated, followed by a reduction to below basal levels in response to treatment with the DNA damaging agents adriamycin and mitomycin C, and that the reduction of BRCA1 expression is dependent on the presence of wild-type p53 ... Ectopic expression of p53 resulted in a rapid decrease in BRCA1 protein and RNA levels and BRCA1 promoter-driven luciferase activity even in null p21 cells deficient in p53 dependent G ( 1 ) arrest
Arizti et al., Mol Cell Biol 2000 : Tumor suppressor p53 is required to modulate BRCA1 expression ... Here we show that BRCA1 expression levels are down-regulated in response to p53 induction in cells that undergo either growth arrest, senescence, or apoptosis ... Physiological stimuli, such as exposure to DNA damaging agents, also result in negative regulation of BRCA1 levels in a p53 dependent manner prior to causing cell cycle arrest ... In conclusion, the data show that BRCA1 expression levels are controlled by the presence and activity of wild-type p53 and suggest the existence of an intracellular p53/BRCA1 pathway in the response of cells to stress conditions
Aprelikova et al., J Biol Chem 2001 : We find that BRCA1 induction of 14-3-3 sigma requires the presence of wild type p53 and can be regulated by a minimal p53 response element
Fan et al., Oncogene 2001 : The tumor suppressor activity of the BRCA1 gene product is due , in part, to functional interactions with other tumor suppressors, including p53 and the retinoblastoma ( RB ) protein
Takimoto et al., Cancer Biol Ther 2002 : We find that the Xeroderma Pigmentosum Complementation group E ( XPE ) mutated Damaged-DNA binding protein p48 ( DDB2 ) is upregulated by BRCA1 in a p53 dependent manner following UVC, Adriamycin, or Cisplatin exposure ... BRCA1 enhances p53 binding to the DDB2 promoter in vivo as well as p53 dependent transactivation of DDB2 promoter-reporter constructs through a classical p53 DNA responsive element
El-Deiry et al., Cancer Biol Ther 2002 (Breast Neoplasms...) : Some evidence suggests BRCA1 may stabilize p53 and direct regulation of DNA repair genes, although how BRCA1 stabilizes p53 remains unclear and whether BRCA1 can upregulate DNA repair genes in a p53 independent manner remains a possibility
Wu et al., J Biol Chem 2003 : Thus, BRCA2 levels in the cell are regulated by three independent mechanisms in a p53 dependent manner
Ongusaha et al., Oncogene 2003 : The tumor suppressor protein BRCA1 has been shown to enhance p53 transcription, whereas activated p53 represses BRCA1 transcription
Hartman et al., J Mol Med (Berl) 2003 (Breast Neoplasms) : Here we discuss the role of BRCA1 and NER in breast cancer and the interactions of BRCA1 with p53 in breast tumorigenesis and suggest approaches for risk assessment and chemotherapeutic management of BRCA1 related breast cancer
Jeffy et al., Neoplasia (New York, N.Y.) 2005 : An estrogen receptor-alpha/p300 complex activates the BRCA-1 promoter at an AP-1 site that binds Jun/Fos transcription factors : repressive effects of p53 on BRCA-1 transcription ... Conversely, we document that overexpression of wild-type p53 prevents the recruitment of ER alpha to the AP-1 site and represses BRCA-1 promoter activity
Honrado et al., Crit Rev Oncol Hematol 2006 (Breast Neoplasms) : BRCA1tumors have been found to be more frequently estrogen receptor- and progesterone receptor negative, and p53 positive than are age matched controls , whereas these differences are not usually found in BRCA2 associated tumors
Buck et al., Cancer Lett 2008 (Breast Neoplasms) : Expression of a truncated BRCA1 ( amino acids 772-1292 ) stimulated p53 DNA binding and transcription activities and apoptosis, recapitulating some effects of DNA damage