Abstract
DNA double strand break repair in mitosis is suppressed by phosphorylation of XRCC4.
Highlights
Cells are continuously subjected to DNA damage, the most cytotoxic form of which is the DNA double-strand break (DSB)
classical non-homologous end joining (C-NHEJ), which is active throughout interphase, is considered a rapid but errorprone pathway that rejoins DSB ends with minimal end processing
While repair of DSBs and cell cycle checkpoint arrest in interphase cells is relatively well understood, less is known regarding how cells respond to DSBs that are incurred when cells are in mitosis
Summary
Cells are continuously subjected to DNA damage, the most cytotoxic form of which is the DNA double-strand break (DSB). The main steps in C-NHEJ are detection of the DSB by the Ku heterodimer, followed by recruitment of end-processing factors and the DNA ligase IV-XRCC4-XLF complex. Alt-NHEJ requires end-resection and involves CtIP, XRCC1, and DNA ligase III, but not the C-NHEJ factors [7].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
