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• W2039919399 abstract "In response to UV light single-stranded DNA intermediates coated by RPA are generated, which trigger the ATR-Chk1 checkpoint pathway. Recruitment/activation of several checkpoint proteins at the damaged sites is important for the subsequent cell cycle arrest. Surprisingly, upon UV irradiation, Rad9 and RPA only minimally accumulate at DNA lesions in G2 phase, suggesting that only few single-stranded DNA intermediates are generated. Also, little phosphorylated Chk1 is observed in G2 phase after UV-irradiation, and UV light fails to elicit efficient accumulation of typical DNA damage response proteins at sites of damage in this phase. In contrast, p38 MAPK is phosphorylated in G2 phase cells after UV damage. Interestingly, despite the lack of an obvious activation of the ATR-Chk1 pathway, only the combined inhibition of the ATR- and p38-dependent pathways results in a complete abrogation of the UV-induced G2/M arrest. This suggests that UV light induces less hazardous lesions in G2 phase or lesions created in this phase are less efficiently processed resulting in a low activation of the ATR-Chk1 pathway. UV-induced G2 checkpoint activation in this situation therefore relies on signalling via the p38 MAPK and ATR-Chk1 signalling cascades." @default.
• W2039919399 created "2016-06-24" @default.
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• W2039919399 date "2013-01-01" @default.
• W2039919399 modified "2023-10-16" @default.
• W2039919399 title "UV-induced G2 checkpoint depends on p38 MAPK and minimal activation of ATR-Chk1 pathway" @default.
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• W2039919399 doi "https://doi.org/10.1242/jcs.118265" @default.
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