APE1 deficiency promotes cellular senescence and premature aging features
Abstract
Base excision repair (BER) handles many forms of endogenous DNA damage, and apurinic/apyrimidinic endonuclease 1 (APE1) is central to this process. Deletion of both alleles of APE1 (a.k.a. Apex1) in mice leads to embryonic lethality, and deficiency in cells can promote cell death. Unlike most other BER proteins, APE1 expression is inversely correlated with cellular senescence in primary human fibroblasts. Depletion of APE1 via shRNA induced...
Paper Details
Title
APE1 deficiency promotes cellular senescence and premature aging features
Published Date
May 10, 2018
Journal
Volume
46
Issue
11
Pages
5664 - 5677
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