Establishment of Cellular Quiescence Together with H2AX Downregulation and Genome Stability Maintenance
Received Date: Jan 15, 2018 / Accepted Date: Jan 18, 2018 / Published Date: Jan 22, 2018
Abstract
H2AX is required for genome stability. In response to DNA double-strand breaks (DSBs), H2AX is rapidly phosphorylated to form γH2AX foci, which mediate DNA repair and checkpoint signaling. This process is regulated by modifications and molecular interactions of H2AX. In addition, the rapid stabilization of H2AX in response to DSBs facilitates γH2AX foci formation. Although H2AX is markedly downregulated in many cellular states, γH2AX foci can still efficiently form upon DSB generation. Here, we review the regulation of H2AX in response to DSBs.
Keywords: H2AX; γH2AX; DNA double-strand breaks
Citation: Matsuno Y, Torigoe H, Yoshioka K (2018) Establishment of Cellular Quiescence Together with H2AX Downregulation and Genome Stability Maintenance. J Clin Exp Pathol 8: 335. Doi: 10.4172/2161-0681.1000335
Copyright: ©2018 Matsuno Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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