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Acyl-Coenzyme A thioesterase 11 (ACOT11) is an enzyme encoded by the ACOT11 gene, primarily responsible for hydrolyzing medium- and long-chain fatty acyl-CoA esters into free fatty acids and coenzyme A. This activity regulates intracellular fatty acid and CoA pools, impacting lipid metabolism, energy expenditure, and membrane synthesis. ACOT11 contains a steroidogenic acute regulatory (StAR)-related lipid transfer (START) domain, allowing lipid sensing and transfer, and is particularly active in brown adipose tissue where it modulates fatty acid oxidation and lipid storage in response to cold exposure. Altered ACOT11 activity is implicated in metabolic diseases, cancer proliferation, and liver steatosis. The enzyme forms homodimers or higher order oligomers and is subject to regulation by post-translational modifications and lipid binding within its START domain. Alternative splicing creates distinct isoforms with tissue and functional specificity. There are no approved drugs targeting ACOT11, nor validated clinical biomarkers for its function.
Enzymes hydrolyze long-chain fatty acyl-CoAs to free fatty acids and CoA, regulating intracellular fatty acid levels and supporting lipid storage or β-oxidation suppression. Drugs (or small molecules if validated in the future) would act as inhibitors or activators altering this enzymatic activity but none are documented in clinical use.
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