Disease on EC 3.1.2.20 - acyl-CoA hydrolase and Organism(s) Homo sapiens and UniProt Accession O00154
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DISEASE 
TITLE OF PUBLICATION
LINK TO PUBMED
acyl-coa hydrolase deficiency
Targeted deletion of thioesterase superfamily member 1 promotes energy expenditure and protects against obesity and insulin resistance.
Adenocarcinoma of Lung
ACOT11 promotes cell proliferation, migration and invasion in lung adenocarcinoma.
Adenocarcinoma of Lung
Overexpression and proliferation dependence of acyl-CoA thioesterase 11 and 13 in lung adenocarcinoma.
Carcinoma
ACOT11 promotes cell proliferation, migration and invasion in lung adenocarcinoma.
Carcinoma, Squamous Cell
ACOT11 promotes cell proliferation, migration and invasion in lung adenocarcinoma.
Colonic Neoplasms
Exosomal miR-183-5p Shuttled by M2 Polarized Tumor-Associated Macrophage Promotes the Development of Colon Cancer via Targeting THEM4 Mediated PI3K/AKT and NF-?B Pathways.
Dyslexia
Lack of association between genetic polymorphisms in ROBO1, MRPL19/C2ORF3 and THEM2 with Developmental Dyslexia.
Dyslexia
The chromosome 6p22 haplotype associated with dyslexia reduces the expression of KIAA0319, a novel gene involved in neuronal migration.
Dyslipidemias
Thioesterase Superfamily Member 2 Promotes Hepatic VLDL Secretion by Channeling Fatty Acids into Triglyceride Biosynthesis.
Fatty Liver
Acyl coenzyme A thioesterase Them5/Acot15 is involved in cardiolipin remodeling and fatty liver development.
Fatty Liver
Phosphatidylcholine transfer protein/StarD2 promotes microvesicular steatosis and liver injury in murine experimental steatohepatitis.
Fatty Liver
Upregulation of Thioesterase Superfamily Member 2 in Skeletal Muscle Promotes Hepatic Steatosis and Insulin Resistance.
Infections
Weighted gene co-expression network analysis and drug-gene interaction bioinformatics uncover key genes associated with various presentations of malaria infection in African children and major drug candidates.
Insulin Resistance
Targeted deletion of thioesterase superfamily member 1 promotes energy expenditure and protects against obesity and insulin resistance.
Insulin Resistance
Thioesterase superfamily member 2 promotes hepatic insulin resistance in the setting of glycerol-3-phosphate acyltransferase 1-induced steatosis.
Insulin Resistance
Upregulation of Thioesterase Superfamily Member 2 in Skeletal Muscle Promotes Hepatic Steatosis and Insulin Resistance.
Liver Diseases
Upregulation of Thioesterase Superfamily Member 2 in Skeletal Muscle Promotes Hepatic Steatosis and Insulin Resistance.
Lung Neoplasms
ACOT11 promotes cell proliferation, migration and invasion in lung adenocarcinoma.
Neoplasms
ACOT11 promotes cell proliferation, migration and invasion in lung adenocarcinoma.
Neoplasms
Comprehensive genome methylation analysis in bladder cancer;identification and validation of novel methylated genes and application of these as urinary tumor markers.
Non-alcoholic Fatty Liver Disease
Thioesterase Superfamily Member 2 Promotes Hepatic VLDL Secretion by Channeling Fatty Acids into Triglyceride Biosynthesis.
Non-alcoholic Fatty Liver Disease
Upregulation of Thioesterase Superfamily Member 2 in Skeletal Muscle Promotes Hepatic Steatosis and Insulin Resistance.
Obesity
Thioesterase superfamily member 1 suppresses cold thermogenesis by limiting the oxidation of lipid droplet-derived fatty acids in brown adipose tissue.
Obesity
Thioesterase Superfamily Member 2 Promotes Hepatic VLDL Secretion by Channeling Fatty Acids into Triglyceride Biosynthesis.
Obesity
Upregulation of Thioesterase Superfamily Member 2 in Skeletal Muscle Promotes Hepatic Steatosis and Insulin Resistance.
Overnutrition
Thioesterase-mediated control of cellular calcium homeostasis enables hepatic ER stress.
Tuberculosis
Identification of a type III thioesterase reveals the function of an operon crucial for Mtb virulence.
Tuberculosis
Insights into the Substrate Specificity of a Thioesterase Rv0098 of Mycobacterium Tuberculosis through X-ray Crystallographic and Molecular Dynamics Studies.
Tuberculosis
Structure based drug discovery for designing leads for the non-toxic metabolic targets in multi drug resistant Mycobacterium tuberculosis.
