期刊
TRENDS IN CELL BIOLOGY
卷 31, 期 10, 页码 843-855出版社
CELL PRESS
DOI: 10.1016/j.tcb.2021.06.002
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资金
- Kids Cancer Alliance, a translational cancer research center of the Cancer Institute NSW
- Australian National Health & Medical Research Council [1162886, 1185870, 2004430]
- Australian Research Council [DP210103885]
- National Health and Medical Research Council of Australia [2004430, 1185870, 1162886] Funding Source: NHMRC
This study focuses on the role of nuclear-specific filamentous actin in mobilizing damaged chromatin in response to DNA double-strand breaks and replication stress, as well as the importance of nuclear pore complexes and promyelocytic leukemia-nuclear bodies as specialized platforms for homology-directed repair. The literature suggests an emerging model where specific types of DNA lesions are subjected to nuclear-derived forces that promote interaction with repair hubs to facilitate specialized repair reactions.
The nucleus is a dynamic environment containing chromatin, membraneless organelles, and specialized molecular structures at the nuclear membrane. Within the spectrum of DNA repair activities are observations of increased mobility of damaged chromatin and the displacement of DNA lesions to specific nuclear environments. Here, we focus on the role that nuclear-specific filamentous actin plays in mobilizing damaged chromatin in response to DNA double-strand breaks and replication stress. We also examine nuclear pore complexes and promyelocytic leukemia-nuclear bodies as specialized platforms for homology-directed repair. The literature suggests an emerging model where specific types of DNA lesions are subjected to nuclear-derived forces that mobilize damaged chromatin and promote interaction with repair hubs to facilitate specialized repair reactions.
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