THE ROLE OF RAD9 IN HEAD AND NECK CANCER
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- ISHIKAWA Kazuhiro
- Department of Otolaryngology-Head and Neck Surgery
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- ISHII Hideshi
- Center for Molecular Medicine, Jichi Medical University School of Medicine
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- NISHINO Hiroshi
- Department of Otolaryngology-Head and Neck Surgery
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- FURUKAWA Yusuke
- Center for Molecular Medicine, Jichi Medical University School of Medicine
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- ICHIMURA Keiichi
- Department of Otolaryngology-Head and Neck Surgery
Bibliographic Information
- Other Title
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- P53/P21経路におけるRad9の役割と頭頸部癌への関与
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Abstract
In response to replication perturbation or damage of DNA, cell-cycle checkpoint is activated, which leads to mutually exclusive, two consequences: cell cycle arrest and repair of damaged DNA, or induction of apoptosis. Although previous studies have suggested that a checkpoint molecule, human Rad9, is involved in the process, the exact mechanism remains to be investigated. Here, we studied the role of Rad9 in DNA damage response through the tumor suppressor p53 pathway. Rad9 bound specifically to a p53-consensus DNA-binding sequence in the P21WAF1 promoter, which increased after exposure to UV. The immunoprecipitation and in vitro binding assay indicated p53 associated with Rad9 regardless of phosphorylation status. Taken together with the assessment of immunohistochemistry showing overexpression of Rad9 in head and neck squamous cell carcinoma cell line, the present study demonstrates overexpression of Rad9 leads to dysregulation of checkpoint response after DNA damage occurs in head and neck cancer.
Journal
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- Toukeibu Gan
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Toukeibu Gan 32 (4), 417-422, 2006
Japan Society for Head and Neck Cancer
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Keywords
Details
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- CRID
- 1390282680198492544
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- NII Article ID
- 10018452628
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- NII Book ID
- AA11985555
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- ISSN
- 18818382
- 13495747
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- Text Lang
- ja
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed