期刊
CURRENT OPINION IN CELL BIOLOGY
卷 24, 期 3, 页码 439-447出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2012.03.008
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资金
- Federal European Biochemical Society (FEBS)
- Netherlands Organisation for Scientific Research (NWO-VENI)
- Netherlands Organisation for Scientific Research (NWO-VIDI and NWO-TOP-GO)
- Human Frontier Science Program (HFSP-CDA)
Cells counteract the adverse effects of chromosome breakage by activating the DNA damage response (DDR), which entails a coordinated series of events that regulate cell cycle progression and repair of DNA lesions. The packaging of genomic DNA into condensed, often inaccessible chromatin severely complicates efficient DNA damage repair in living cells. Recent studies implicate a large number of chromatin-modifying enzymes in the DDR, suggesting a stepwise model in which chromatin is continually reconfigured to accommodate the association and action of repair factors during the different stages of the DDR. Emerging evidence suggests that the histone ubiquitin ligases RNF8/RNF168 act in concert with ATP-dependent chromatin remodelling enzymes to orchestrate the signalling and repair of DNA lesions in specific chromatin topologies.
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