BRIP1（BACH1和FANCJ）是抑癌基因，编码蛋白是RecQ DEAH解旋酶家族的成员。DEAH解旋酶参与前信使RNA剪接和核糖体的生物合成。RecQ DEAH解旋酶家族包括与遗传性人类疾病有关的基因，BLM、WRN和RECQL4。具体而言，BRIP1与BRCA1的BRCT结构域相互作用。BRIP1 p.K52R的突变可以控制这两种蛋白质的相互作用。BRIP1已被证明在遗传性乳腺癌、卵巢癌和前列腺癌以及Fanconi anemia (FA)中发生突变。FA是由DNA修复中的一些基因缺陷引起的一种紊乱，其特征是骨髓衰竭、对DNA交联剂敏感,FA患者往往容易诱发的癌症是急性髓细胞性白血病（AML）。BRIP1缺乏的细胞系对丝裂霉素C（交联剂）敏感。

BRIP1 (BACH1 and FANCJ) is a member of the RecQ DEAH helicase family. DEAH helicases participate in pre-messenger RNA splicing and ribosome biogenesis. This family of genes includes those that have been implicated in heritable human diseases, including BLM, WRN and RECQL4. Specifically, BRIP1 interacts with the BRCT motif-containing domain of BRCA1. In the HCC1937 cell line that produces BRCA1 with a truncated C-terminal, BRIP1 failed to co-immunoprecipitate with BRCA1, suggesting this domain is important for interaction with BRIP1. In the same study, two intact BRCT repeat units on BRCA1 were shown to be necessary for the BRCA1 and BRIP1 interaction; a mutation at K52R on BRIP1 may control the interaction of the two proteins. BRIP1 has been shown to be mutated in hereditary breast, ovarian and prostate cancers as well as the Fanconi anemia (FA), a disorder caused by genetic defects in a number of proteins involved in DNA repair that is characterized by bone marrow failure, sensitivity to DNA cross-linking agents and the development of cancer, often acute myelogenous leukemia (AML). Cell lines that are deficient in BRIP1 are sensitive to mitomycin C, a crosslinking agent.

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