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In addition, we worked on two human breast cancer susceptibility genes, BRCA1 & BRCA2 and have established their dual participation in transcription regulation and DNA damage repair. BRCA1 has been shown to associate directly with the RAD50/MRE11/NBS1 complex, which functions in both non-homologous end-joining and homologous recombination repair of DNA double-strand breaks. The BRCA2 via its BRC repeats binds to RAD51, which catalyzes homologous DNA pairing and DNA strand exchange in an in vitro recombination reaction. Expression of a wild-type BRC repeat disrupted this interaction and rendered cells hypersensitive to gamma-irradiation and failed to activate the G2/M checkpoint. Small molecules that disrupt the interaction between BRC repeat and Rad51 have been isolated. These small compounds offer a potential to develop new combinatorial treatment with chemotherapy or radiation therapy.
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