Journal
JOURNAL OF CELL BIOLOGY
Volume 217, Issue 1, Pages 21-37Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201706061
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Funding
- National Institutes of Health, National Cancer Institute
- Center for Cancer Research
- Progeria Research Foundation
- NATIONAL CANCER INSTITUTE [ZIABC010309] Funding Source: NIH RePORTER
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Despite the extensive description of numerous molecular changes associated with aging, insights into the driver mechanisms of this fundamental biological process are limited. Based on observations in the premature aging syndrome Hutchinson-Gilford progeria, we explore the possibility that protein regulation at the inner nuclear membrane and the nuclear lamina contributes to the aging process. In support, sequestration of nucleoplasmic proteins to the periphery impacts cell stemness, the response to cytotoxicity, proliferation, changes in chromatin state, and telomere stability. These observations point to the nuclear periphery as a central regulator of the aging phenotype.
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