MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan
Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is sho...
Ausführliche Beschreibung
Autor*in: |
Mingfu Tian [verfasserIn] Yuqing Huang [verfasserIn] Yunting Song [verfasserIn] Wen Li [verfasserIn] Peiyi Zhao [verfasserIn] Weiyong Liu [verfasserIn] Kailang Wu [verfasserIn] Jianguo Wu [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2020 |
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Schlagwörter: |
Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) |
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Übergeordnetes Werk: |
In: Advanced Science - Wiley, 2015, 7(2020), 22, Seite n/a-n/a |
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Übergeordnetes Werk: |
volume:7 ; year:2020 ; number:22 ; pages:n/a-n/a |
Links: |
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DOI / URN: |
10.1002/advs.202001950 |
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Katalog-ID: |
DOAJ016966570 |
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520 | |a Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. | ||
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10.1002/advs.202001950 doi (DE-627)DOAJ016966570 (DE-599)DOAJa9a33fd1858441768e95312338c9cf57 DE-627 ger DE-627 rakwb eng Mingfu Tian verfasserin aut MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. aging DNA repair Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) senescence senescence‐associated secretory phenotype (SASP) Science Q Yuqing Huang verfasserin aut Yunting Song verfasserin aut Wen Li verfasserin aut Peiyi Zhao verfasserin aut Weiyong Liu verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/article/a9a33fd1858441768e95312338c9cf57 kostenfrei https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a |
spelling |
10.1002/advs.202001950 doi (DE-627)DOAJ016966570 (DE-599)DOAJa9a33fd1858441768e95312338c9cf57 DE-627 ger DE-627 rakwb eng Mingfu Tian verfasserin aut MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. aging DNA repair Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) senescence senescence‐associated secretory phenotype (SASP) Science Q Yuqing Huang verfasserin aut Yunting Song verfasserin aut Wen Li verfasserin aut Peiyi Zhao verfasserin aut Weiyong Liu verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/article/a9a33fd1858441768e95312338c9cf57 kostenfrei https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a |
allfields_unstemmed |
10.1002/advs.202001950 doi (DE-627)DOAJ016966570 (DE-599)DOAJa9a33fd1858441768e95312338c9cf57 DE-627 ger DE-627 rakwb eng Mingfu Tian verfasserin aut MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. aging DNA repair Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) senescence senescence‐associated secretory phenotype (SASP) Science Q Yuqing Huang verfasserin aut Yunting Song verfasserin aut Wen Li verfasserin aut Peiyi Zhao verfasserin aut Weiyong Liu verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/article/a9a33fd1858441768e95312338c9cf57 kostenfrei https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a |
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10.1002/advs.202001950 doi (DE-627)DOAJ016966570 (DE-599)DOAJa9a33fd1858441768e95312338c9cf57 DE-627 ger DE-627 rakwb eng Mingfu Tian verfasserin aut MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. aging DNA repair Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) senescence senescence‐associated secretory phenotype (SASP) Science Q Yuqing Huang verfasserin aut Yunting Song verfasserin aut Wen Li verfasserin aut Peiyi Zhao verfasserin aut Weiyong Liu verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In Advanced Science Wiley, 2015 7(2020), 22, Seite n/a-n/a (DE-627)817357777 (DE-600)2808093-2 21983844 nnns volume:7 year:2020 number:22 pages:n/a-n/a https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/article/a9a33fd1858441768e95312338c9cf57 kostenfrei https://doi.org/10.1002/advs.202001950 kostenfrei https://doaj.org/toc/2198-3844 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2020 22 n/a-n/a |
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Mingfu Tian |
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Mingfu Tian misc aging misc DNA repair misc Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) misc senescence misc senescence‐associated secretory phenotype (SASP) misc Science misc Q MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan |
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MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan aging DNA repair Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) senescence senescence‐associated secretory phenotype (SASP) |
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misc aging misc DNA repair misc Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) misc senescence misc senescence‐associated secretory phenotype (SASP) misc Science misc Q |
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misc aging misc DNA repair misc Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1) misc senescence misc senescence‐associated secretory phenotype (SASP) misc Science misc Q |
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MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan |
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mysm1 suppresses cellular senescence and the aging process to prolong lifespan |
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MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan |
abstract |
Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. |
abstractGer |
Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. |
abstract_unstemmed |
Abstract Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases. |
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MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan |
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