TY - JOUR
T1 - DNA damage and decisions
T2 - CtIP coordinates DNA repair and cell cycle checkpoints
AU - You, Zhongsheng
AU - Bailis, Julie M.
N1 - Funding Information:
We apologize to colleagues whose work we were not able to cite in this review owing to space limitations. We thank Drs. Tony Hunter, Helen Piwnica-Worms, Tony Polverino and Susana Gonzalo for critical reading of the manuscript and their insightful input. Research in Z.Y.’s lab is supported by startup funds from the Department of Cell Biology and Physiology at Washington University School of Medicine, a grant from the American Cancer Society (IRG-58-010-52) and a Washington University Molecular Imaging Center Pilot Research Project grant.
PY - 2010/7
Y1 - 2010/7
N2 - Maintenance of genome stability depends on efficient, accurate repair of DNA damage. DNA double-strand breaks (DSBs) are among the most lethal types of DNA damage, with the potential to cause mutation, chromosomal rearrangement, and genomic instability that could contribute to cancer. DSB damage can be repaired by various pathways including nonhomologous end-joining (NHEJ) and homologous recombination (HR). However, the cellular mechanisms that regulate the choice of repair pathway are not well understood. Recent studies suggest that the tumor suppressor protein CtIP controls the decision to repair DSB damage by HR. It does so by regulating the initiation of DSB end resection after integrating signals from the DNA damage checkpoint response and cell cycle cues.
AB - Maintenance of genome stability depends on efficient, accurate repair of DNA damage. DNA double-strand breaks (DSBs) are among the most lethal types of DNA damage, with the potential to cause mutation, chromosomal rearrangement, and genomic instability that could contribute to cancer. DSB damage can be repaired by various pathways including nonhomologous end-joining (NHEJ) and homologous recombination (HR). However, the cellular mechanisms that regulate the choice of repair pathway are not well understood. Recent studies suggest that the tumor suppressor protein CtIP controls the decision to repair DSB damage by HR. It does so by regulating the initiation of DSB end resection after integrating signals from the DNA damage checkpoint response and cell cycle cues.
UR - http://www.scopus.com/inward/record.url?scp=77954313601&partnerID=8YFLogxK
U2 - 10.1016/j.tcb.2010.04.002
DO - 10.1016/j.tcb.2010.04.002
M3 - Review article
C2 - 20444606
AN - SCOPUS:77954313601
SN - 0962-8924
VL - 20
SP - 402
EP - 409
JO - Trends in Cell Biology
JF - Trends in Cell Biology
IS - 7
ER -