PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30510203-6 2018 Gene ontology pathway analysis revealed Sirt3 deletion-mediated downregulation of enzymes in several metabolic pathways, including fatty acid oxidation and tricarboxylic acid cycle. Tricarboxylic Acids 156-174 sirtuin 3 Mus musculus 40-45 25948682-5 2015 Permeabilized muscle fibers from HFD-fed SIRT3 knockout (KO) mice showed that tricarboxylic acid cycle substrate-based respiration is decreased while fatty acid-based respiration is increased, reflecting a fuel switch from glucose to fatty acids. Tricarboxylic Acids 78-96 sirtuin 3 Mus musculus 41-46 23576753-7 2013 These data show that SIRT3 regulates acetylation on multiple proteins, often at multiple sites, across several metabolic pathways including fatty acid oxidation, ketogenesis, amino acid catabolism, and the urea and tricarboxylic acid cycles, as well as mitochondrial regulatory proteins. Tricarboxylic Acids 215-233 sirtuin 3 Mus musculus 21-26 33531400-4 2021 Infection of immortalized and primary murine macrophages resulted in reduced levels of SIRT3 mRNA and protein and perturbation of SIRT3-regulated enzymes in the tricarboxylic acid cycle, electron transport chain, and glycolytic pathway. Tricarboxylic Acids 161-179 sirtuin 3 Mus musculus 130-135 32526680-0 2020 Sirt3 is a novel target to treat sepsis induced myocardial dysfunction by acetylated modulation of critical enzymes within cardiac tricarboxylic acid cycle. Tricarboxylic Acids 131-149 sirtuin 3 Mus musculus 0-5 32526680-7 2020 Quantitative acetyl-proteomics and cardiac metabolomics analysis revealed that loss of Sirt3 led to hyper-acetylation of critical enzymes within cardiac tricarboxylic acid (TCA) cycle and generation of lactate and NADH, subsequently promotion of cardiac dysfunction after sepsis. Tricarboxylic Acids 153-171 sirtuin 3 Mus musculus 87-92 32526680-7 2020 Quantitative acetyl-proteomics and cardiac metabolomics analysis revealed that loss of Sirt3 led to hyper-acetylation of critical enzymes within cardiac tricarboxylic acid (TCA) cycle and generation of lactate and NADH, subsequently promotion of cardiac dysfunction after sepsis. Tricarboxylic Acids 173-176 sirtuin 3 Mus musculus 87-92