文献类型： 外文期刊
作者： Peng, X-J. 1 ; Liu, S-J. 1 ; Bao, C-M. 1 ; Liu, Y-Z. 1 ; Xie, H-W. 3 ; Cai, Y-H. 4 ; Li, B-M. 1 ; Hang, H-Y.; Ding, X. 1 ;
作者机构： 1.Nanchang Univ, Sch Life Sci, Nanchang 330031, Jiangxi, Peoples R China
2.Nanchang Univ, Inst Life Sci, Nanchang 330031, Jiangxi, Peoples R China
3.Jiangxi Acad Agr Sci, Jiangxi Super Rice Res & Dev Ctr, Nanchang 330031, Jiangxi, Peoples R China
4.Jiangxi Acad Agr Sci, Jiangxi Super Rice Res & Dev Ctr,
关键词： DNA damage signaling;ATRIP;RAD9;Cell cycle checkpoints;Genome stability
期刊名称：CELLULAR AND MOLECULAR BIOLOGY （ 影响因子：1.77； 五年影响因子：1.695 ）
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收录情况： SCI
摘要： Genotoxic stress activates checkpoint signaling pathways that activate the checkpoint kinases ATM and ATR, halt cell cycle progression, and promote DNA repair. A number of proteins act in concert with ATR to phosphorylate Chk1, including RAD17, the RAD9-RAD1-HUS1 complex, ATR/ATRIP and TopBp1. However, how these proteins involved act in concert with one another to propagate and maintain the checkpoint response is not well understood. Here, we reported that upregulation of RAD9 protein increased the quantity of ATRIP, suggesting that RAD9 activation will induce more efficient accumulation of ATRIP in vivo. Furthermore, the DNA damage-induced ATRIP foci formation was faster in the mRad9(-/-) ES cells. Also, ATRIP interacts specifically with RAD9, but not HUS1 and RAD1. Taken together, we suggested that RAD9 could affect both the ATRIP protein levels and DNA damage-induced ATRIP foci formation. Thus, we propose a role of RAD9 in the ATR-Chk1 pathway that is necessary for successful formation of the damage-sensing complex and DNA damage checkpoint signaling.
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