A major switch for the Fanconi anemia DNA damage-response pathway.
Wang
Weidong
W
Laboratory of Genetics, National Institute on Aging, National Institutes of Health, NIH Biomedical Research Center, Room 10B113, 251 Bayview Boulevard, Baltimore, Maryland 21224, USA. wangw@grc.nia.nih.gov
D000818:Animals; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D005199:Fanconi Anemia / Q000235:genetics / Q000378:metabolism; D051856:Fanconi Anemia Complementation Group Proteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*
D018797:Cell Cycle Proteins; C519921:FANCI protein, human; D051856:Fanconi Anemia Complementation Group Proteins; C576597:ATR protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases