Target：ACAT-1

Fields：Fatty acid degradation;Valine, leucine and isoleucine degradation;Lysine degradation;Tryptophan metabolism;Pyruvate metabolism;Glyoxylate and dicarboxylate metabolism;Butanoate metabolism;Terpenoid backbone biosynthesis;Metabolic pathways;Carbon metabolism;Fatty acid metabolism;Fat digestion and absorption

Gene Name：ACAT1

Protein Name：Acetyl-CoA acetyltransferase mitochondrial

Human Gene Id：38

Human Swiss Prot No：P24752

Mouse Gene Id：110446

Mouse Swiss Prot No：Q8QZT1

Rat Gene Id：25014

Rat Swiss Prot No：P17764

Immunogen：The antiserum was produced against synthesized peptide derived from human ACAT1. AA range:221-270

Specificity：ACAT-1 Polyclonal Antibody detects endogenous levels of ACAT-1 protein.

Formulation：Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Source：Polyclonal, Rabbit,IgG

Dilution：WB 1:500 - 1:2000. IHC 1:100 - 1:300. ELISA: 1:40000.. IF 1:50-200

Purification：The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Concentration：1 mg/ml

Storage Stability：-15°C to -25°C/1 year(Do not lower than -25°C)

Other Name：ACAT1;ACAT;MAT;Acetyl-CoA acetyltransferase; mitochondrial;Acetoacetyl-CoA thiolase;T2

Observed Band(KD)：45kD

Background： This gene encodes a mitochondrially localized enzyme that catalyzes the reversible formation of acetoacetyl-CoA from two molecules of acetyl-CoA. Defects in this gene are associated with 3-ketothiolase deficiency, an inborn error of isoleucine catabolism characterized by urinary excretion of 2-methyl-3-hydroxybutyric acid, 2-methylacetoacetic acid, tiglylglycine, and butanone. [provided by RefSeq, Feb 2009],

Function：catalytic activity:2 acetyl-CoA = CoA + acetoacetyl-CoA.,disease:Defects in ACAT1 are a cause of 3-ketothiolase deficiency (3KTD) [MIM:203750]; also known as alpha-methylacetoaceticaciduria. 3KTD is an inborn error of isoleucine catabolism characterized by intermittent ketoacidotic attacks associated with unconsciousness. Some patients die during an attack or are mentally retarded. Urinary excretion of 2-methyl-3-hydroxybutyric acid, 2-methylacetoacetic acid, triglylglycine, butanone is increased. It seems likely that the severity of this disease correlates better with the environmental or acquired factors than with the ACAT1 genotype.,enzyme regulation:Activated by potassium ions, but not sodium ions.,function:Plays a major role in ketone body metabolism.,similarity:Belongs to the thiolase family.,subunit:Homotetramer.,

Subcellular Location：Mitochondrion .

Expression： Adipocyte,Brain,Fetal brain cortex,