机构:
Univ Michigan, Sch Med, Div Mol Med & Genet, Dept Internal Med, Ann Arbor, MI 48109 USAUniv Michigan, Sch Med, Div Mol Med & Genet, Dept Internal Med, Ann Arbor, MI 48109 USA
Liu, Zixing
[1
]
Wu, Jiaxue
论文数: 0引用数: 0
h-index: 0
机构:
Univ Michigan, Sch Med, Div Mol Med & Genet, Dept Internal Med, Ann Arbor, MI 48109 USAUniv Michigan, Sch Med, Div Mol Med & Genet, Dept Internal Med, Ann Arbor, MI 48109 USA
Wu, Jiaxue
[1
]
Yu, Xiaochun
论文数: 0引用数: 0
h-index: 0
机构:
Univ Michigan, Sch Med, Div Mol Med & Genet, Dept Internal Med, Ann Arbor, MI 48109 USAUniv Michigan, Sch Med, Div Mol Med & Genet, Dept Internal Med, Ann Arbor, MI 48109 USA
Yu, Xiaochun
[1
]
机构:
[1] Univ Michigan, Sch Med, Div Mol Med & Genet, Dept Internal Med, Ann Arbor, MI 48109 USA
Breast cancer-1 (BRCA1) participates in the DNA damage response. However, the mechanism by which BRCA1 is recruited to DNA damage sites remains elusive. Recently, we have demonstrated that a ubiquitin-binding protein, RAP80, is required for DNA damage-induced BRCA1 translocation. Here we identify another component, CCDC98, in the BRCA1-RAP80 complex. CCDC98 mediates BRCA1's association with RAP80. Moreover, CCDC98 controls both DNA damage-induced formation of BRCA1 foci and BRCA1-dependent G2/M checkpoint activation. Together, our results demonstrate that CCDC98 is a BRCA1 binding partner that mediates BRCA1 function in response to DNA damage.