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Updated: Jan 24, 2026

Comparison of Three Different Methods for Determining Cell Proliferation in Breast Cancer Cell Lines
Published on: September 3, 2016
CtIP is essential for early B cell proliferation and development in mice
Xiangyu Liu1,2, Xiaobin S Wang1,3, Brian J Lee1
1Institute for Cancer Genetics, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY.
Abstract:
B cell development requires efficient proliferation and successful assembly and modifications of the immunoglobulin gene products. CtIP is an essential gene implicated in end resection and DNA repair. Here, we show that CtIP is essential for early B cell development but dispensable in naive B cells. CtIP loss is well tolerated in G1-arrested B cells and during V(D)J recombination, but in proliferating B cells, CtIP loss leads to a progressive cell death characterized by ATM hyperactivation, G2/M arrest, genomic instability, and 53BP1 nuclear body formation, indicating that the essential role of CtIP during proliferation underscores its stage-specific requirement in B cells. B cell proliferation requires phosphorylation of CtIP at T847 presumably by CDK, but not its interaction with CtBP or Rb or its nuclease activity. CtIP phosphorylation by ATM/ATR at T859 (T855 in mice) promotes end resection in G1-arrested cells but is dispensable for B cell development and class switch recombination, suggesting distinct roles for T859 and T847 phosphorylation in B cell development.
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