Muscle-specific knockout of general control of amino acid synthesis 5 (GCN5) does not enhance basal or endurance exercise-induced mitochondrial adaptation.

Jessica R Dent,Vitor F Martins,Kristoffer Svensson,Samuel A LaBarge, Noah C Schlenk,Mary C Esparza,Elisa H Buckner,Gretchen A Meyer,D Lee Hamilton,Simon Schenk,Andrew Philp

Molecular Metabolism（2017）

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摘要

•Development of a novel muscle-specific GCN5 knockout (mKO) mouse model.•GCN5 mKO does not affect body composition or 24 h whole-body metabolism.•GCN5 mKO mice do not exhibit changes in basal mitochondrial abundance or respiratory capacity.•Exercise-induced mitochondrial biogenesis in skeletal muscle is not enhanced in GCN5 mKO mice.

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关键词

Acetylation,GCN5,Mitochondria,SIRT1,Deacetylase,PGC-1α

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