◀ Back to BRCA1

BRCA1 — E2F4

Pathways - manually collected, often from reviews:

• FastForward regulation: E2F4 → BRCA1 (transcriptional regulation, unknown) Cam et al., Mol Cell 2004
  Evidence: DNABINDING

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: BRCA1 — E2F4 Wang et al., Oncogene 1997
• IRef Bind_translation Interaction: BRCA1 — E2F4 (affinity chromatography technology) Wang et al., Oncogene 1997
• IRef Biogrid Interaction: BRCA1 — E2F4 (direct interaction, pull down) Wang et al., Oncogene 1997
• IRef Hprd Interaction: BRCA1 — E2F4 (in vitro) Wang et al., Oncogene 1997
• IRef Hprd Interaction: BRCA1 — E2F4 (in vivo) Wang et al., Oncogene 1997
• IRef Innatedb Interaction: Complex of 13 proteins (unknown, -) Bindra et al., Cancer Res 2005*
• IRef Innatedb Interaction: BRCA1 — E2F4 (unknown, -) Bindra et al., Cancer Res 2005*
• IRef Ophid Interaction: BRCA1 — E2F4 (aggregation, confirmational text mining) Wang et al., Oncogene 1997
• IRef Ophid Interaction: BRCA1 — E2F4 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Wang et al., J Biol Chem 2000 (Breast Neoplasms...) : Moreover, ectopic expression of cyclin D1 and Cdk4 can stimulate the Brca1 promoter in an E2F dependent manner, and this is inhibited by coexpression of the p16(INK4a) cyclin dependent kinase inhibitor
Bindra et al., Cancer Biol Ther 2006 (Breast Neoplasms...) : We have shown recently that the tumor microenvironmental stress of hypoxia induces an E2F dependent repression of BRCA1 in cancer cells ... In contrast to previous studies, we have also detected promoter occupancy by the pocket proteins p130 and p107, but not Rb, our data indicate that E2F4 and p130/p107 complexes basally repress the BRCA1 promoter