作者: Nobuko Matsushita , Hiroyuki Kitao , Masamichi Ishiai , Naoki Nagashima , Seiki Hirano
DOI: 10.1016/J.MOLCEL.2005.08.018
关键词: FANCG 、 Biology 、 FANCD2 、 FAN1 、 DNA repair 、 Molecular biology 、 Cell biology 、 Chromatin 、 Fusion protein 、 Fanconi anemia, complementation group C 、 Monoubiquitination
摘要: In DNA damage responses, the Fanconi anemia (FA) protein, FancD2, is targeted to chromatin and forms nuclear foci following its monoubiquitination, a process likely catalyzed by FA core complex. Here, we show that chicken FancD2-ubiquitin fusion carrying Lys-Arg substitution removing natural monoubiquitination site (D2KR-Ub), could reverse cisplatin hypersensitivity localize in FANCD2-deficient DT40 cells. Importantly, targeting was dependent on three complex components as well hydrophobic surface of ubiquitin may direct protein-protein interactions. Furthermore, constitutively bound D2KR-histone H2B complement sensitivity FANCD2- but not FANCC-, FANCG-, or FANCL-deficient Thus these have an additional function repair, which independent FancD2. These results define functional consequences FancD2 reveal previously hidden functions for protein