2011
DOI: 10.1073/pnas.1102789108
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Abstract: Specific point mutations in lamin A gene have been shown to accelerate aging in humans and mice. Particularly, a de novo mutation at G608G position impairs lamin A processing to produce the mutant protein progerin, which causes the Hutchinson Gilford progeria syndrome. The premature aging phenotype of Hutchinson Gilford progeria syndrome is largely recapitulated in mice deficient for the lamin A-processing enzyme, Zmpste24. We have previously reported that Zmpste24 deficiency results in genomic instability and… Show more

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Cited by 202 publications
(166 citation statements)
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“…The hyperacetylation paradigm runs counter to observations that histone deacetylase inhibitors can enhance healthspan and longevity (Krishnan et al, 2011;Zhao et al, 2005). It is becoming evident that histone acetylation plays a more nuanced role in gene regulation, with site specific changes in histone acetylation playing just as important a role as more global alterations (Peleg et al, 2016).…”
Section: Accepted M Manuscriptmentioning
confidence: 80%
“…The hyperacetylation paradigm runs counter to observations that histone deacetylase inhibitors can enhance healthspan and longevity (Krishnan et al, 2011;Zhao et al, 2005). It is becoming evident that histone acetylation plays a more nuanced role in gene regulation, with site specific changes in histone acetylation playing just as important a role as more global alterations (Peleg et al, 2016).…”
Section: Accepted M Manuscriptmentioning
confidence: 80%
“…Butyrate is a general HDAC inhibitor and protects against high‐fat diet‐induced metabolic changes (Gao et al ., 2009), has anti‐inflammatory properties (Maslowski et al ., 2009) and extends lifespan in a mouse model of progeria (Krishnan et al ., 2011) and Drosophila (Zhao et al ., 2005). Thus, we hypothesized that butyrate would improve metabolism and prevent muscle atrophy in mice during aging.…”
Section: Introductionmentioning
confidence: 99%
“…Recently, histone acetylation at H4-K16 by the MYST family HAT MOF was reported to be required for the recruitment of repair factors, such as MDC1, 53BP1 and BRCA1, to an irradiation-induced DSB site. This acetylation may be a key regulator for DSB repair pathway choice between HR and NHEJ during the S to G2 phase of the cell cycle (Li et al, 2010;Krishnan et al, 2011;Gupta et al, 2014).…”
Section: Introductionmentioning
confidence: 99%