Atsushi Shibata

TL;DR: Evidence is presented that following exposure to ionising radiation, γH2AX foci analysis can provide a sensitive monitor of DSB formation and repair and techniques to optimise the analysis are described, enabling the procedure to be optimally exploited but not misused.

TL;DR: It is shown that in G2, as in G1, NHEJ represents the major DSB‐repair pathway whereas HR is only essential for repair of ∼15% of X‐ or γ‐ray‐induced DSBs.

TL;DR: This work employed structure-based design with a focused chemical library to discover specific MRE11 endo- or exonuclease inhibitors and define distinct nuclease roles in DSB repair, and support a mechanism whereby M RE11 endonucleasing initiates resection, thereby licensing HR followed by MRE 11 exonuclelease and EXO1/BLM bidirectional resection toward and away from the DNA end, which commits to HR.

TL;DR: It is proposed that NHEJ initially attempts to repair DSBs and, if rapid rejoining does not ensue, then resection occurs promoting repair by HR, and novel roles for ATM in regulating DSB end resection are identified.

TL;DR: The involvement of DSB repair in PD-L1 expression is revealed and mechanistic insight is provided into howPD-L 1 expression is regulated after DSBs, which requires ATM/ATR/Chk1 kinases and IRF1 signalling.