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Literature summary for 2.3.1.48 extracted from

  • Dent, J.R.; Martins, V.F.; Svensson, K.; LaBarge, S.A.; Schlenk, N.C.; Esparza, M.C.; Buckner, E.H.; Meyer, G.A.; Hamilton, D.L.; Schenk, S.; Philp, A.
    Muscle-specific knockout of general control of amino acid synthesis 5 (GCN5) does not enhance basal or endurance exercise-induced mitochondrial adaptation (2017), Mol. Metab., 6, 1574-1584 .
    View publication on PubMedView publication on EuropePMC
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Cloned(Commentary)

Cloned (Comment) Organism
gene GCN5, enzyme expression analysis Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information generation of mKO mice, mice harboring LoxP sites flanking exons 3-19 of the GCN5 gene, referred to as GCN5flox/flox, usage of Cre-LoxP methodology to generate mice with muscle-specific knockout of GCN5 (mKO) and floxed, wildtype littermates. Despite successful knockdown of GCN5 activity in skeletal muscle of mKO mice, whole-body energy expenditure as well as skeletal muscle mitochondrial abundance and maximal respiratory capacity are comparable between mKO and wild-type mice. No differences in skeletal muscle expression of several genes between wild-type and GCN5 mKO mice, overview. Skeletal muscle gene expression of metabolic, angiogenic, and mitochondrial genes is not affected by loss of GCN5. Loss of GCN5 does not alter body composition, in vivo metabolism or energy expenditure Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
-
 Mus musculus 5739
-
nucleus
-
 Mus musculus 5634
-

Organism

Organism UniProt Comment Textmining
Mus musculus Q9JHD2
-
-

Source Tissue

Source Tissue Comment Organism Textmining
additional information enzyme GCN5 expression analysis in different tissues from fasted (4 h) and anesthetized mice, overview Mus musculus
-
skeletal muscle
-
 Mus musculus
-

Synonyms

Synonyms Comment Organism
Gcn5
-
 Mus musculus
general control of amino acid synthesis 5
-
 Mus musculus
HAT
-
 Mus musculus

General Information

General Information Comment Organism
malfunction loss of GCN5 in vivo does not promote metabolic remodeling in mouse skeletal muscle. Skeletal muscle gene expression of metabolic, angiogenic, and mitochondrial genes is not affected by loss of GCN5. Loss of GCN5 does not affect myosin heavy chain (MHC) composition, and markers of skeletal muscle development are unaffected by loss of GCN5. Skeletal muscle maximal respiratory capacity and succinate dehydrogenase (SDH) enzyme activity are not affected by loss of GCN5. Loss of GCN5 does not affect mitochondrial content or adaptations to endurance exercise training Mus musculus
physiological function lysine acetyltransferase GCN5 is a regulator of mitochondrial biogenesis via its inhibitory action on peroxisome proliferator activated receptor-gamma coactivator-1alpha (PGC-1alpha). Specific contribution of GCN5 to skeletal muscle metabolism and mitochondrial adaptations to endurance exercise in vivo Mus musculus