期刊
BMB REPORTS
卷 44, 期 5, 页码 352-357出版社
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2011.44.5.352
关键词
Ataxia telangiectasia and Rad3-related protein (ATR); Checkpoint kinase 1 (Chk1); Human MutY homolog (hMYH); Hydroxyurea (HU); Ultraviolet (UV)
资金
- National Research Foundation of Korea (NRF) [2010-0016187]
- Kyung Hee University [KHU-20100159]
- Korean Ministry of Science and Technology
- WCU (World Class University) [R33-2008-000-1071]
- Ministry of Education, Science and Technology
The effect of human MutY homolog (hMYH) on the activation of checkpoint proteins in response to hydroxyurea (HU) and ultraviolet (UV) treatment was investigated in hMYH-disrupted HEK293 cells. hMYH-disrupted cells decreased the phosphorylation of Chk1 upon HU or UV treatment and increased the phosphorylation of Cdk2 and the amount of Cdc25A, but not Cdc25C. In siMYH-transfected cells, the increased rate of phosphorylated Chk1 upon HU or UV treatment was lower than that in siGFP-transfected cells, meaning that hMYH was involved in the activation mechanism of Chk1 upon DNA damage. The phosphorylation of ataxia telangiectasia and Rad3-related protein (AIR) upon HU or UV treatment was decreased in hMYH-disrupted HEK293 and HaCaT cells. Co-immunoprecipitation experiments showed that hMYH was immunoprecipitated by anti-AIR. These results suggest that hMYH may interact with ATR and function as a mediator of Chk1 phosphorylation in response to DNA damage. [BMB reports 2011; 44(5): 352-357]
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