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Prepublished online as a Blood First Edition Paper on June 28, 2002; DOI 10.1182/blood-2002-01-0278. This Article Full Text (PDF) All Versions of this Article: 2002-01-0278v1 100/7/2414    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Taniguchi, T. Articles by D'Andrea, A. D Search for Related Content PubMed PubMed Citation Articles by Taniguchi, T. Articles by D'Andrea, A. D Social Bookmarking                   What's this? Submitted January 30, 2002 Accepted April 5, 2002 S phase-specific interaction of the Fanconi anemia protein, FANCD2, with BRCA1 and RAD51 Toshiyasu Taniguchi, Irene Garcia-Higuera, Paul R Andreassen, Richard C Gregory, Markus Grompe, and Alan D D'Andrea* Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Harvard Medical School, Boston, MA, USA Department of Molecular and Medical Genetics and Department of Pediatrics, Oregon Health Sciences University, Portland, OR, USA Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Pediatrics, Children's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA * Corresponding author; email: alan_dandrea{at}dfci.harvard.edu. Fanconi Anemia (FA) is a human autosomal recessive cancer susceptibility disorder characterized by cellular sensitivity to Mitomycin C and defective cell cycle progression. Six FA genes (corresponding to subtypes A, C, D2, E, F, and G) have been cloned, and the encoded FA proteins interact in a common pathway. DNA damage activates this pathway, leading to the monoubiquitination of the downstream FANCD2 protein and its targeting to nuclear foci containing BRCA1. In the current study, we demonstrate that FANCD2 also undergoes monoubiquitination during S phase of the cell cycle. Monoubiquitinated FANCD2 colocalizes with BRCA1 and RAD51 in S phase-specific nuclear foci. Monoubiquitination of FANCD2 is required for normal cell cycle progression following cellular exposure to Mitomycin C. Our data indicate that the monoubiquitination of FANCD2 is highly regulated and suggest that FANCD2/BRCA1 complexes and FANCD2/RAD51 complexes participate in an S phase specific cellular process, such as DNA repair by homologous recombination. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. 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