期刊
MOLECULAR CELL
卷 32, 期 6, 页码 767-777出版社
CELL PRESS
DOI: 10.1016/j.molcel.2008.12.003
关键词
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资金
- AICR (Association for International Cancer Research) UK
- MRC [MC_U105178811, MC_U105185859] Funding Source: UKRI
- Medical Research Council [MC_U105178811, MC_U105185859] Funding Source: researchfish
A key step in the Fanconi anemia (FA) tumor suppressor pathway is the site-specific monoubiquitination of the FANCD2 protein. Genetic studies indicate that this crucial modification requires eight known FA gene products and the E2-conjugating enzyme Ube2t. Here, we minimally reconstitute this monoubiquitination reaction with Ube2t and the FANCL protein, revealing that monoubiquitination is stimulated by a conserved RWD-like domain in FANCL. Furthermore, addition of the FANCI protein enhances monoubiquitination and also restricts it to the in vivo substrate lysine residue on FANCD2. This work therefore establishes a system that provides mechanistic insight into the functions of FANCL and FANCI in the catalysis of FANCD2 monoubiquitination.
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