Journal
INTERNATIONAL JOURNAL OF HEMATOLOGY
Volume 93, Issue 4, Pages 417-424Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s12185-011-0777-z
Keywords
Fanconi anemia; Interstrand crosslink; The FA pathway; DNA repair; DNA damage signaling
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Funding
- 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
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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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