期刊
INTERNATIONAL JOURNAL OF HEMATOLOGY
卷 93, 期 4, 页码 417-424出版社
SPRINGER JAPAN KK
DOI: 10.1007/s12185-011-0777-z
关键词
Fanconi anemia; Interstrand crosslink; The FA pathway; DNA repair; DNA damage signaling
类别
资金
- Ministry of Education, Science, Sports, and Culture of Japan
- The Uehara Memorial Foundation
- Takeda foundation
- Grants-in-Aid for Scientific Research [21590338, 23651046] Funding Source: KAKEN
Fanconi anemia (FA) is a cancer predisposition disorder characterized by progressive bone marrow failure, congenital developmental defects, chromosomal abnormalities, and cellular hypersensitivity to DNA interstrand crosslink (ICL) agents. So far mutations in 14 FANC genes were identified in FA or FA-like patients. These gene products constitute a common ubiquitin-phosphorylation network called the FA pathway and cooperate with other proteins involved in DNA repair and cell cycle control to repair ICL lesions and to maintain genome stability. In this review, we summarize recent exciting discoveries that have expanded our view of the molecular mechanisms operating in DNA repair and DNA damage signaling.
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