دورية أكاديمية
Knock-down of human MutY homolog (hMYH) decreases phosphorylation of checkpoint kinase 1 (Chk1) induced by hydroxyurea and UV treatment
العنوان: | Knock-down of human MutY homolog (hMYH) decreases phosphorylation of checkpoint kinase 1 (Chk1) induced by hydroxyurea and UV treatment |
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المساهمون: | Soo-Hyun Hahm, Jong-Hwa Park, Sung Il Ko, You Ri Lee, In Sik Chung, Ji Hyung Chung, Lin-Woo Kang, Ye Sun Han, Chung, Ji Hyung |
المصدر: | T201103293.pdf |
سنة النشر: | 2011 |
مصطلحات موضوعية: | Animals, Ataxia Telangiectasia Mutated Proteins, Cell Cycle Proteins/genetics, Cell Cycle Proteins/metabolism, Cell Line, Checkpoint혻Kinase혻1, 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, Small Interfering/metabolism, Ultraviolet Rays, Ataxia telangiectasia and Rad3-related protein (ATR), Checkpoint kinase 1 (Chk1), Human MutY homolog (hMYH), Hydroxyurea (HU), Ultraviolet (UV) |
الوصف: | 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 ; open |
نوع الوثيقة: | article in journal/newspaper |
وصف الملف: | 352~357 |
اللغة: | unknown |
تدمد: | 1976-6696 1976-670X |
العلاقة: | BMB REPORTS; J00348; OAK-2011-01623; https://ir.ymlib.yonsei.ac.kr/handle/22282913/94149Test; T201103293; BMB REPORTS, Vol.44(5) : 352-357, 2011 |
DOI: | 10.5483/BMBRep.2011.44.5.352 |
الإتاحة: | https://doi.org/10.5483/BMBRep.2011.44.5.352Test https://ir.ymlib.yonsei.ac.kr/handle/22282913/94149Test |
حقوق: | CC BY-NC-ND 2.0 KR ; https://creativecommons.org/licenses/by-nc-nd/2.0/krTest/ ; free |
رقم الانضمام: | edsbas.5B89FACA |
قاعدة البيانات: | BASE |
تدمد: | 19766696 1976670X |
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DOI: | 10.5483/BMBRep.2011.44.5.352 |