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BRCA1 — E2F4
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 *
-
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