【摘 要】
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To minimize the toxic insults of DNA double strand break (DSB), organisms have developed three efficient repair pathways: Homologous Recombination (HR), Non
【机 构】
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CollegeofLifeSciences,ZhejiangUniversity,866YuHangTangRoad,Hangzhou310058
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To minimize the toxic insults of DNA double strand break (DSB), organisms have developed three efficient repair pathways: Homologous Recombination (HR), Non-Homologous End Joining (NHEJ), Single-Strand Annealing (SSA).A central part of DNA damage response is activation of tumour repressor p53 resulting in cell cycle arrest, DNA damage repair, apoptosis, or senescense to guard the genome stability.Surprisingly p53 inhibits DNA DSB repair.There are various p53 isoforms in vivo.However, information on the functions of the p53 isoforms in DNA damage repair is lacking.Our previous studies showed that an N-terminal truncated p53, △113p53/△133p53 is a p53 target gene, which is strongly induced by DNA damage signals.In this study, we found that △113p53 is only induced by ionizing irradiation, but not by UV irradiation and heat shock.
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