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Knock-down of human MutY homolog (hMYH) decreases phosphorylation of checkpoint kinase 1 (Chk1) induced by hydroxyurea and UV treatment

Authors
 Soo-Hyun Hahm  ;  Jong-Hwa Park  ;  Sung Il Ko  ;  You Ri Lee  ;  In Sik Chung  ;  Ji Hyung Chung  ;  Lin-Woo Kang  ;  Ye Sun Han 
Citation
 BMB REPORTS, Vol.44(5) : 352-357, 2011 
Journal Title
BMB REPORTS
ISSN
 1976-6696 
Issue Date
2011
MeSH
Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line ; CheckpointKinase1 ; DNA Damage/drug effects ; DNA Glycosylases/genetics ; DNA Glycosylases/metabolism* ; Enzyme Inhibitors/pharmacology ; Gene Knockdown Techniques ; Humans ; Hydroxyurea/pharmacology* ; Phosphorylation/drug effects* ; Phosphorylation/radiation effects* ; Protein Kinases/genetics ; Protein Kinases/metabolism* ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Ultraviolet Rays*
Keywords
Ataxia telangiectasia and Rad3-related protein (ATR) ; Checkpoint kinase 1 (Chk1) ; Human MutY homolog (hMYH) ; Hydroxyurea (HU) ; Ultraviolet (UV)
Abstract
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 (ATR) upon HU or UV treatment was decreased in hMYH-disrupted HEK293 and HaCaT cells. Co-immunoprecipitation experiments showed that hMYH was immunoprecipitated by anti-ATR. These results suggest that hMYH may interact with ATR and function as a mediator of Chk1 phosphorylation in response to DNA damage
Files in This Item:
T201103293.pdf Download
DOI
10.5483/BMBRep.2011.44.5.352
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
Yonsei Authors
Chung, Ji Hyung(정지형)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/94149
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