DNA double-strand breaks(DSBs)severely impact the integrity of the genome and cell homeostasis.To address DSBs,cells activate sophisticated mechanisms to repair this DNA damage.Non-homologous end joining(NHEJ)is a pre...DNA double-strand breaks(DSBs)severely impact the integrity of the genome and cell homeostasis.To address DSBs,cells activate sophisticated mechanisms to repair this DNA damage.Non-homologous end joining(NHEJ)is a predominant pathway for repairing DSBs.p53 binding protein 1(53BP1)serves as a pivotal regulator in the NHEJ pathway.By locating and forming phase separation at DSB sites,53BP1 acts as a scaffold protein to recruit downstream components and facilitate DSB repair[1].展开更多
基金supported by the National Natural Science Foundation of China(32422041,32071226)the Foundation of Hubei Hongshan Laboratory(2021HSZD011)+1 种基金the Fundamental Research Funds for the Central Universities(2662023PY001)the HZAU-AGIS Cooperation Fund(SZYJY2022022).
文摘DNA double-strand breaks(DSBs)severely impact the integrity of the genome and cell homeostasis.To address DSBs,cells activate sophisticated mechanisms to repair this DNA damage.Non-homologous end joining(NHEJ)is a predominant pathway for repairing DSBs.p53 binding protein 1(53BP1)serves as a pivotal regulator in the NHEJ pathway.By locating and forming phase separation at DSB sites,53BP1 acts as a scaffold protein to recruit downstream components and facilitate DSB repair[1].
