{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:05:42Z","timestamp":1791396342512,"version":"4.3.3"},"reference-count":0,"publisher":"National Academy of Sciences","issue":"17","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1994,8,16]]},"abstract":"<jats:p>Features of chromosomal aberrations, hypersensitivity to DNA crosslinking agents, and predisposition to malignancy have suggested a fundamental anomaly of DNA repair in Fanconi anemia. The function of the recently isolated FACC (Fanconi anemia group C complementing) gene for a subset of this disorder is not yet known. The notion that FACC plays a direct role in DNA repair would predict that the polypeptide should reside in the nucleus. In this study, a polyclonal antiserum raised against FACC was used to determine the subcellular location of the polypeptide. Immunofluorescence and subcellular fractionation studies of human cell lines as well as COS-7 cells transiently expressing human FACC showed that the protein was localized primarily to the cytoplasm under steady-state conditions, transit through the cell cycle, and exposure to crosslinking or cytotoxic agents. However, placement of a nuclear localization signal from the simian virus 40 large tumor antigen at the amino terminus of FACC directed the hybrid protein to the nuclei of transfected COS-7 cells. These observations suggest an indirect role for FACC in regulating DNA repair in this group of Fanconi anemia.<\/jats:p>","DOI":"10.1073\/pnas.91.17.7975","type":"journal-article","created":{"date-parts":[[2006,5,31]],"date-time":"2006-05-31T08:52:13Z","timestamp":1149065533000},"page":"7975-7979","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":106,"title":["Localization of Fanconi anemia C protein to the cytoplasm of mammalian cells."],"prefix":"10.1073","volume":"91","author":[{"given":"H","family":"Youssoufian","sequence":"first","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1994,8,16]]},"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.91.17.7975","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,13]],"date-time":"2022-04-13T13:52:29Z","timestamp":1649857949000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/full\/10.1073\/pnas.91.17.7975"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,8,16]]},"references-count":0,"journal-issue":{"issue":"17","published-print":{"date-parts":[[1994,8,16]]}},"alternative-id":["10.1073\/pnas.91.17.7975"],"URL":"https:\/\/doi.org\/10.1073\/pnas.91.17.7975","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,8,16]]},"assertion":[{"value":"1994-08-16","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}