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      Protein sequestration at the nuclear periphery as a potential regulatory mechanism in premature aging

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      The Journal of Cell Biology

      The Rockefeller University Press

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          Abstract

          Serebryannyy and Misteli provide a perspective on how protein sequestration at the inner nuclear membrane and nuclear lamina might influence aging.

          Abstract

          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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          Most cited references 274

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          Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Wnt/β-catenin signaling and disease.

            The WNT signal transduction cascade controls myriad biological phenomena throughout development and adult life of all animals. In parallel, aberrant Wnt signaling underlies a wide range of pathologies in humans. In this Review, we provide an update of the core Wnt/β-catenin signaling pathway, discuss how its various components contribute to disease, and pose outstanding questions to be addressed in the future. Copyright © 2012 Elsevier Inc. All rights reserved.
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               D. Harman (1956)
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                Author and article information

                Journal
                J Cell Biol
                J. Cell Biol
                jcb
                jcb
                The Journal of Cell Biology
                The Rockefeller University Press
                0021-9525
                1540-8140
                2 January 2018
                : 217
                : 1
                : 21-37
                Affiliations
                National Cancer Institute, National Institutes of Health, Bethesda, MD
                Author notes
                Correspondence to Tom Misteli: mistelit@ 123456mail.nih.gov ;
                Article
                201706061
                10.1083/jcb.201706061
                5748986
                29051264
                This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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                Funding
                Funded by: National Institutes of Health, DOI https://doi.org/10.13039/100000002;
                Funded by: National Cancer Institute, DOI https://doi.org/10.13039/100000054;
                Funded by: Center for Cancer Research
                Funded by: Progeria Research Foundation, DOI https://doi.org/10.13039/100002287;
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                Cell biology

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