Home > Browse Issues > Vol.39 No.11
The Mechanism of ATM Regulating Somatic Cell Reprogramming
He Haipeng, Wu Xia*
State Key Laboratory of Reproductive Regulation & Breeding of Grassland Livestock, College of Biosciences, Inner Mongolia University, Hohhot 010021, China
Abstract: Ataxia telangiectasia mutated (ATM)， as a member of the phosphatidylinositol-3-kinase related kinase family (PIKK)， is a DNA-damaging sensor. It transmits DNA damage signals to DNA repair proteins， activates several signal pathways， such as DNA repair， cell cycle blockage， apoptosis and so on， in order to repair DNA damages and keep genomic integrality. Recently， ATM was known to be involved in somatic reprogramming by transcriptional factors. During the process， ATM knock-out significantly affected final generation of induced pluripotent stem cells (iPS cells)， and increased the chances of abnormal chromosomes in these iPS cells. In addition， ATM also took part in chromatin remodeling during somatic reprogramming. Furthermore， downstream effectors of ATM， such as p53 and H2AX (histone 2A member X)， regulated the reprogramming-activated cell cycle blockage and apoptosis. For the theoretical supports of improving iPS cells research in future， the aim of this review is to provide a systematic overview on the mechanism of ATM and its downstream effectors in regulating somatic reprogramming.
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