| Literature DB >> 34915311 |
Chuanming Dong1, Xianli Wang2, Lixin Sun3, Liang Zhu3, Danjing Yang3, Shane Gao3, Wenjun Zhang4, Bin Ling5, Aibin Liang6, Zhengliang Gao7, Jun Xu8.
Abstract
Ataxia telangiectasia mutated (ATM) plays an essential role in DNA damage response and the maintenance of genomic stability. However, the role of ATM in regulating the function of adult neural stem cells (NSCs) remains unclear. Here we report that ATM deficiency led to accumulated DNA damage and decreased DNA damage repair capacity in neural progenitor cells. Moreover, we observed ATM ablation lead to the short-term increase of proliferation of neural progenitor cells, resulting in the depletion of the NSC pool over time, and this loss of NSC quiescence resulted in accelerated cell senescence. We further apply RNA sequencing to unravel that ATM knockout significantly affected Notch signaling pathway, furthermore, notch activation inhibit the abnormal increased proliferation of ATM-/- NSCs. Taken together, these findings indicate that ATM can serve as a key regulator for the normal function of adult NSCs by maintaining their stemness and preventing cellular senescence primarily through Notch signaling pathway.Entities:
Keywords: ATM; Aging; Neural stem cell; Notch signaling pathway; Quiescence
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Year: 2021 PMID: 34915311 DOI: 10.1016/j.scr.2021.102618
Source DB: PubMed Journal: Stem Cell Res ISSN: 1873-5061 Impact factor: 2.020