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BRCA1 — CDK1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: BRCA1 → CDK1 (increases)
  Evidence: We found that the number of cells containing at least five BRCA1 foci was reduced 2.8-fold in the absence of cdk1 in untreated cells, and by 3.7-fold (p = 0.00075) at 6 hr after IR treatment (Figure 3B).

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: CDK1 — BRCA1 Wang et al., Oncogene 1997
• IRef Bind_translation Interaction: CDK1 — BRCA1 (affinity chromatography technology) Wang et al., Oncogene 1997
• IRef Biogrid Interaction: BRCA1 — CDK1 (direct interaction, pull down) Wang et al., Oncogene 1997
• IRef Hprd Interaction: CDK1 — BRCA1 (in vivo) Wang et al., Oncogene 1997
• IRef Hprd Interaction: CDK1 — BRCA1 (in vitro) Wang et al., Oncogene 1997
• IRef Ophid Interaction: CDK1 — BRCA1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Ouchi et al., Proc Natl Acad Sci U S A 2000 : After IFN-gamma treatment, induction of the cyclin dependent kinase inhibitor, p21WAF1, was synergistically activated by BRCA1 , whereas the IRF-1 gene was unaffected
Sankaran et al., Cancer Res 2007 : We show that Aurora-A kinase modulates the BRCA1 inhibition of centrosome function by decreasing the E3 ubiquitin ligase activity of BRCA1
Johnson et al., Nat Med 2011 (Breast Neoplasms...) : Because reduced Cdk1 activity impaired BRCA1 function and consequently, repair by homologous recombination, inhibition of Cdk1 represents a plausible strategy for expanding the utility of PARP inhibitors to BRCA-proficient cancers