UV-induced G2 checkpoint depends on p38 MAPK and minimal activation of ATR-Chk1 pathway

摘要: In response to UV light, single-stranded DNA intermediates coated with replication protein A (RPA) are generated, which trigger the ATR-Chk1 checkpoint pathway. Recruitment and/or activation of several proteins at damaged sites is important for subsequent cell cycle arrest. Surprisingly, upon irradiation, Rad9 and RPA only minimally accumulate lesions in G2 phase, suggesting that a few generated. Also, little phosphorylated Chk1 observed phase after UV-irradiation, light fails elicit efficient accumulation typical damage this phase. By contrast, p38 MAPK cells damage. Interestingly, despite lack an obvious pathway, combined inhibition ATR- p38-dependent pathways results complete abrogation UV-induced G2/M This suggests induces less hazardous or created efficiently processed, resulting low situation therefore relies on signalling via cascades.