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Altered endocytosis in cellular senescence
Affiliation:1. Department of Biochemistry, Chungbuk National University College of Medicine, Cheongju, 28644, South Korea;2. World Class Institute, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Ochang-eup, Cheongju, 28116, South Korea;3. Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, And Department of Cell Biology, Yale University School of Medicine, New Haven, CT, 06511, USA;4. Wellcome Trust Centre for Cell-matrix Research, University of Manchester, Manchester, UK
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.
Keywords:Endocytosis  Senescence  Caveolin-1  Amphiphysin  βPAK-interacting nucleotide exchange factor (βPIX)  ING1
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