Gene interactions and pathways from curated databases and text-mining

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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 *

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