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FLASH GENE
Symbol ACAT2 contributors: mct - updated : 31-08-2010
HGNC name acetyl-Coenzyme A acetyltransferase 2
HGNC id 94
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a thiolase domain
  • C-terminal end is the putative active site domain due to its high degree of sequence conservation from yeast to humans (Das 2008)
    • mono polymer homomer , tetramer
    HOMOLOGY
    interspecies homolog to rattus Acat2 (86.87 pc)
    homolog to murine Acat2 (87.12 pc)
    Homologene
    FAMILY
  • thiolase family
    • CATEGORY enzyme , regulatory
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,cytosolic
    basic FUNCTION
  • catalyzes the synthesis of cholesteryl esters from cholesterol and long-chain fatty acids (Pramfalk 2007)
  • acetoacetyl-CoA thiolase 2, playing a catalytic role in fetal liver and in intestinal enterocytes
  • promotes cholesterol absorption by the intestine and the secretion of cholesteryl ester-enriched very low density lipoproteins by the liver (Alger 2010)
  • plays a critical role in the production of atherogenic apoB-containing lipoproteins (Alger 2010)
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism lipid/lipoprotein
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • binding
    • cell & other
    REGULATION
    Other regulated by HNF4alpha (important regulator of the hepatocyte-specific expression of the human ACAT2 promoter) (Pramfalk 2009)
    transcriptionally regulated by cholesterol(Pramfalk 2007)
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility coronary artey disease risk and high plasma lipid levels
    Variant & Polymorphism polymorphisms associated with CAD risk and plasma lipid levels
    Candidate gene
    Marker
    Therapy target
  • target for prevention and treatment of hypercholesterolemia and atherosclerosis
  • ACAT2-specific inhibitors may hold unexpected therapeutic potential to treat both atherosclerosis and non-alcoholic fatty liver disease (Alger 2010)
    • ANIMAL & CELL MODELS
    mice genetically lacking ACAT2 in both the intestine and the liver were dramatically protected against hepatic neutral lipid (TG and cholesteryl ester) accumulation, with the greatest differences occurring in situations where dietary cholesterol was elevated (Alger 2010)