Brca1 CKO Mouse Model

The mutation in tumor suppressor gene BRCA1 is the most common contributor to human genetic cancers and can cause breast or ovarian cancers. BCRA1 protein is involved in a large number of important cellular processes, including transcriptional regulation, chromatin remodeling, cell cycle regulation, and the repair of double-stranded DNA. When an endogenous error occurs in DNA replication or when DNA is exposed to a genotoxic agent, ubiquitin ligase can be directly activated by post-translational modification of BRCA1/BARD1, thereby generating an appropriate response to DNA damages, increasing the stability of the genome, and ultimately inhibiting tumor formation.

Due to growth retardation, neural tube defects and mesoderm abnormalities, homozygous mice carrying systemic Brca1 knockout frequently suffer from embryonic death. In contrary, the conditional knockout promotes tumor formation. The truncation mutation of BRCA1 protein in mice can cause twisted tail, abnormal pigmentation, male infertility and an increased incidence of tumor.

Our own-developed Brca1 conditional knockout mice (Brca1-CKO) can be used to study breast cancer.

Fig1. The BRCA1 network. （Nat Rev Cancer. 2004 Sep;4(9):665-76.）