a DNA-dependent ATPase and DNA helicase required for the maintenance of chromosomal stability. Involved in the repair of DNA double-strand breaks by homologous recombination in a manner that depends on its association with BRCA1. Binds directly to the BRCT domains of BRCA1. Defects in BRIP1 cause of susceptibility to breast cancer and Fanconi anemia. Acts late in the Fanconi anemia pathway, after FANCD2 ubiquitination. Belongs to the DEAD box helicase family, DEAH subfamily. Two alternatively spliced human isoforms have been described. Note: This description may include information from UniProtKB.
Molecular Function: 4 iron, 4 sulfur cluster binding; ATP binding; ATP-dependent DNA helicase activity; DNA binding; metal ion binding; protein binding
Biological Process: DNA damage checkpoint; DNA duplex unwinding; DNA repair; double-strand break repair; double-strand break repair via homologous recombination; double-strand break repair via synthesis-dependent strand annealing; negative regulation of cell proliferation; regulation of transcription from RNA polymerase II promoter
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.