TY - JOUR
T1 - Fanconi anemia (cross)linked to DNA repair
AU - Niedernhofer, Laura J.
AU - Lalai, Astrid S.
AU - Hoeijmakers, Jan H.J.
N1 - Funding Information:
We apologize for the limited number of references due to space limitations. A.S.L. and J.H.J.H. are supported by the Dutch Cancer Society, the EC, the NIH, and the Netherlands Organization for Scientific Research (NWO). L.J.N. is supported by the University of Pittsburgh Cancer Institute and the NCI (K22-CA111525).
PY - 2005/12/29
Y1 - 2005/12/29
N2 - Fanconi anemia is characterized by hypersensitivity to DNA interstrand crosslinks (ICLs) and susceptibility to tumor formation. Despite the identification of numerous Fanconi anemia (FANC) genes, the mechanism by which proteins encoded by these genes protect a cell from DNA interstrand crosslinks remains unclear. The recent discovery of two DNA helicases that, when defective, cause Fanconi anemia tips the balance in favor of the direct involvement of the FANC proteins in DNA repair and the bypass of DNA lesions.
AB - Fanconi anemia is characterized by hypersensitivity to DNA interstrand crosslinks (ICLs) and susceptibility to tumor formation. Despite the identification of numerous Fanconi anemia (FANC) genes, the mechanism by which proteins encoded by these genes protect a cell from DNA interstrand crosslinks remains unclear. The recent discovery of two DNA helicases that, when defective, cause Fanconi anemia tips the balance in favor of the direct involvement of the FANC proteins in DNA repair and the bypass of DNA lesions.
UR - http://www.scopus.com/inward/record.url?scp=29244489543&partnerID=8YFLogxK
U2 - 10.1016/j.cell.2005.12.009
DO - 10.1016/j.cell.2005.12.009
M3 - Review article
C2 - 16377561
AN - SCOPUS:29244489543
SN - 0092-8674
VL - 123
SP - 1191
EP - 1198
JO - Cell
JF - Cell
IS - 7
ER -