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BRCA1 — FANCD2
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:
FANCD2
—
BRCA1
Garcia-Higuera et al., Mol Cell 2001, Taniguchi et al., Blood 2002*
-
IRef Bind_translation Interaction:
FANCD2
—
BRCA1
(unspecified method)
Taniguchi et al., Blood 2002*
-
IRef Bind_translation Interaction:
FANCD2
—
BRCA1
(coimmunoprecipitation)
Garcia-Higuera et al., Mol Cell 2001, Taniguchi et al., Blood 2002*
-
IRef Biogrid Interaction:
FANCD2
—
BRCA1
(direct interaction, enzymatic study)
Vandenberg et al., Mol Cell 2003*
-
IRef Biogrid Interaction:
FANCD2
—
BRCA1
(direct interaction, two hybrid)
Reuter et al., Exp Cell Res 2003
-
IRef Biogrid Interaction:
FANCD2
—
BRCA1
(physical association, affinity chromatography technology)
Garcia-Higuera et al., Mol Cell 2001
-
IRef Hprd Interaction:
FANCD2
—
BRCA1
(in vivo)
Garcia-Higuera et al., Mol Cell 2001
-
IRef Intact Interaction:
FANCD2
—
BRCA1
(colocalization, fluorescence microscopy)
Garcia-Higuera et al., Mol Cell 2001
-
IRef Intact Interaction:
FANCD2
—
BRCA1
(physical association, coimmunoprecipitation)
Garcia-Higuera et al., Mol Cell 2001
-
IRef Ophid Interaction:
FANCD2
—
BRCA1
(aggregation, confirmational text mining)
Garcia-Higuera et al., Mol Cell 2001
-
IRef Ophid Interaction:
FANCD2
—
BRCA1
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Vandenberg et al., Mol Cell 2003
(Fanconi Anemia) :
Consequently, while
BRCA1 affects the accumulation of
FANCD2 at sites of DNA damage, BRCA1/BARD1 E3 ligase activity is not essential for the monoubiquitination of FANCD2
Bogliolo et al., EMBO J 2007
(Chromosomal Instability) :
FANCD2 binding to gammaH2AX is
BRCA1 dependent and cells deficient or depleted of H2AX show an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC
Burkitt et al., Cancer Lett 2007
(Carcinoma, Squamous Cell...) :
The defect in FANCD2 foci formation in the cisplatin-sensitive cell lines was not due to defective monoubiquitylation of FANCD2 but appeared to be due to reduced expression or defective function of BRCA1 since expression of exogenous
BRCA1 restored the ability of these cells to induce
FANCD2 foci following cisplatin treatment and enhanced cisplatin resistance
Longerich et al., DNA repair 2008
:
Interestingly, while
Brca1 is
required to recruit ubiquitinated
FancD2 to DNA damage, the phenotype of Brca1-deficient DT40 differs from the one of FancD2-deficient DT40, in which both gene conversion and non templated mutations are impaired