| Literature DB >> 33753287 |
Eun-Young Shin1, Nak-Kyun Soung2, Martin Alexander Schwartz3, Eung-Gook Kim4.
Abstract
Cellular senescence occurs in response to diverse stresses (e.g., telomere shortening, DNA damage, oxidative stress, oncogene activation). A growing body of evidence indicates that alterations in multiple components of endocytic pathways contribute to cellular senescence. Clathrin-mediated endocytosis (CME) and caveolae-mediated endocytosis (CavME) represent major types of endocytosis that are implicated in senescence. More recent research has also identified a chromatin modifier and tumor suppressor that contributes to the induction of senescence via altered endocytosis. Here, molecular regulators of aberrant endocytosis-induced senescence are reviewed and discussed in the context of their capacity to serve as senescence-inducing stressors or modifiers.Entities:
Keywords: Amphiphysin; Caveolin-1; Endocytosis; ING1; Senescence; βPAK-interacting nucleotide exchange factor (βPIX)
Year: 2021 PMID: 33753287 DOI: 10.1016/j.arr.2021.101332
Source DB: PubMed Journal: Ageing Res Rev ISSN: 1568-1637 Impact factor: 10.895