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Hydroxyacyl-coenzyme A dehydrogenase

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Plays an essential role in the mitochondrial beta-oxidation of short chain fatty acids. Exerts it highest activity toward 3-hydroxybutyryl-CoA.

Below are the list of possible Hydroxyacyl-coenzyme A dehydrogenase products. If you cannot find the target and/or product is not available in our catalog, please click here to contact us and request the product or submit your request for custom elisa kit production, custom recombinant protein production or custom antibody production. Custom ELISA Kits, Recombinant Proteins and Antibodies can be designed, manufactured and produced according to the researcher's specifications.
 

Hydroxyacyl-coenzyme A dehydrogenase

 Hydroxyacyl-coenzyme A dehydrogenase ELISA Kit
 Hydroxyacyl-coenzyme A dehydrogenase Recombinant
 Hydroxyacyl-coenzyme A dehydrogenase Antibody
Also known as Hydroxyacyl-coenzyme A dehydrogenase, mitochondrial (HCDH) (Medium and short-chain L-3-hydroxyacyl-coenzyme A dehydrogenase) (Short-chain 3-hydroxyacyl-CoA dehydrogenase).
HADHSC: Plays an essential role in the mitochondrial beta- oxidation of short chain fatty acids. Exerts it highest activity toward 3-hydroxybutyryl-CoA. Defects in HADH are the cause of 3-alpha-hydroxyacyl-CoA dehydrogenase deficiency (HADH deficiency). HADH deficiency is a metabolic disorder with various clinical presentations including hypoglycemia, hepatoencephalopathy, myopathy or cardiomyopathy, and in
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some cases sudden death. Defects in HADH are the cause of familial hyperinsulinemic hypoglycemia type 4 (HHF4); also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. It causes nesidioblastosis, a diffuse abnormality of the pancreas in which there is extensive, often disorganized formation of new islets. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur. HHF4 should be easily recognizable by analysis of acylcarnitine species and that this disorder responds well to treatment with diazoxide. It provides the first 'experiment of nature' that links impaired fatty acid oxidation to hyperinsulinism and that provides support for the concept that a lipid signaling pathway is implicated in the control of insulin secretion. Belongs to the 3-hydroxyacyl-CoA dehydrogenase family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Amino Acid Metabolism - lysine degradation; Amino Acid Metabolism - tryptophan; Amino Acid Metabolism - valine, leucine and isoleucine degradation; Carbohydrate Metabolism - butanoate; EC 1.1.1.35; Lipid Metabolism - fatty acid; Lipid Metabolism - fatty acid elongation in mitochondria; Oxidoreductase

Chromosomal Location of Human Ortholog: 4q22-q26

Cellular Component: cytoplasm; mitochondrial matrix; mitochondrion; nucleoplasm

Molecular Function: 3-hydroxyacyl-CoA dehydrogenase activity

Biological Process: fatty acid beta-oxidation

Disease: 3-hydroxyacyl-coa Dehydrogenase Deficiency; Hyperinsulinemic Hypoglycemia, Familial, 4
 HADH ELISA Kit
 HADH Recombinant
 HADH Antibody
 HAD ELISA Kit
 HAD Recombinant
 HAD Antibody
 HADHSC ELISA Kit
 HADHSC Recombinant
 HADHSC Antibody
 SCHAD ELISA Kit
 SCHAD Recombinant
 SCHAD Antibody
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