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Literature summary for 2.3.1.B43 extracted from

  • Hershberger, K.A.; Abraham, D.M.; Martin, A.S.; Mao, L.; Liu, J.; Gu, H.; Locasale, J.W.; Hirschey, M.D.
    Sirtuin 5 is required for mouse survival in response to cardiac pressure overload (2017), J. Biol. Chem., 292, 19767-19781 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.3.1.B43

Protein Variants

Protein Variants Comment Organism
additional information generation of SIRT5-KO mice. SIRT5-KO mice and wild-type controls undergo transverse aortic constriction (TAC) and are monitored for 16 weeks. In response to TAC, median survival is starkly decreased in SIRT5-KO mice compared with controls. No death is observed in the sham control groups for either genotype. SIRT5-KO mice have impaired systolic function 4 weeks post-TAC. These findings suggest that SIRT5-KO mice progress to cardiac dysfunction at an accelerated rate upon TAC-induced cardiac stress compared with controls, overview. SIRT5-KO mice demonstrate enhanced pathologic concentric hypertrophy in response to pressure overload, with key abnormalities in both cardiac relaxation and performance. Protein succinylation is increased in SIRT5KO hearts and abundant on enzymes in oxidative metabolism Mus musculus

Localization

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

Organism

Organism UniProt Comment Textmining
Mus musculus A0A1Y7VM56
-
-

Source Tissue

Source Tissue Comment Organism Textmining
heart
-
 Mus musculus
-

Synonyms

Synonyms Comment Organism
NAD+-dependent protein deacylase
-
 Mus musculus
SIRT5
-
 Mus musculus
sirtuin 5
-
 Mus musculus

Cofactor

Cofactor Comment Organism Structure
NAD+
-
 Mus musculus

General Information

General Information Comment Organism
malfunction SIRT5-KO mice have reduced survival upon transverse aortic constriction (TAC) compared with wild-type mice but exhibit no mortality when undergoing a sham control operation. The increased mortality with TAC is associated with increased pathological hypertrophy and with key abnormalities in both cardiac performance and ventricular compliance. An accelerated development of cardiac dysfunction in SIRT5KO mice in response to TAC, explaining increased mortality upon cardiac stress. Protein succinylation is increased in SIRT5-KO hearts and abundant on enzymes in oxidative metabolism. SIRT5-KO mouse phenotype, detailed overview Mus musculus
physiological function in mitochondria, the sirtuin SIRT5 is an NAD+-dependent protein deacylase controls several metabolic pathways. A wide range of SIRT5 targets have been identified. SIRT5 functions in organismal metabolic homeostasis. SIRT5 plays a role in cardiac stress responses Mus musculus