Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human HADH Antibodies:
anti-Rat (Rattus) HADH Antibodies:
anti-Mouse (Murine) HADH Antibodies:
Go to our pre-filtered search.
Human Monoclonal HADH Primary Antibody for IF, IHC (p) - ABIN561223
Tönjes, Barbus, Park, Wang, Schlotter, Lindroth, Pleier, Bai, Karra, Piro, Felsberg, Addington, Lemke, Weibrecht, Hovestadt, Rolli, Campos, Turcan, Sturm, Witt, Chan, Herold-Mende, Kemkemer, König et al.: BCAT1 promotes cell proliferation through amino acid catabolism in gliomas carrying wild-type IDH1. ... in Nature medicine 2013
Show all 3 Pubmed References
Human Polyclonal HADH Primary Antibody for ELISA, WB - ABIN262295
Molven, Matre, Duran, Wanders, Rishaug, Njølstad, Jellum, Søvik: Familial hyperinsulinemic hypoglycemia caused by a defect in the SCHAD enzyme of mitochondrial fatty acid oxidation. in Diabetes 2003
The most frequently seen mutations in Turkish patients with congenital hyperinsulinism (CHI) were ATP binding cassette subfamily C (show CYP Antibodies) member 8 (ABCC8 (show ABCC8 Antibodies)) gene, followed by 3-hydroxyacyl CoA dehydrogenase (HADH) and kcnj11 (show KCNJ11 Antibodies) channel (KCNJ11 (show KCNJ11 Antibodies)) genes.
We present clinical and laboratory findings together with the long-term clinical course of a case with a deep intronic HADH (show HADHA Antibodies) splicing mutation (c.636+471G>T) causing neonatal-onset hyperinsulinemic hypoglycemia with mild progression
in a cohort of hyperinsulinemic hypoglycemia patients from Isfahan, Iran, 78% were noted to have disease-causing mutations: 48% had HADH (show HADHA Antibodies) mutations and 26% had ABCC8 (show ABCC8 Antibodies) mutations.
Next-generation sequencing reveals deep intronic cryptic ABCC8 (show ABCC8 Antibodies) and HADH (show HADHA Antibodies) splicing founder mutations causing hyperinsulinism by pseudoexon activation.
Loss of function mutations in 3-Hydroxyacyl-CoA Dehydrogenase (HADH) cause leucine sensitive hyperinsulinaemic hypoglycaemia.
Clinical, biochemical and molecular findings of four new Caucasian patients with HADH (show HADHA Antibodies) deficiency.
We recommend that HADH (show HADHA Antibodies) sequence analysis is considered in all patients with diazoxide-responsive hyperinsulinemic hypoglycemia when recessive inheritance is suspected
Congenital hyperinsulinism due to mutations in HNF4A (show HNF4A Antibodies) and HADH (show HADHA Antibodies).
SCHAD (show HSD17B10 Antibodies) deficiency can result in persistent hyperinsulinemic hypoglycemia of infancy
Unlikely that variation in HADHSC plays a major role in the pathogenesis of type 2 diabetes in the examined cohorts.
A physical association between short-chain 3-hydroxyacyl-coenzyme A dehydrogenase and important components of other key metabolic pathways. Most of the interactions were with enzymes in mitochondrial pathways.
SCHAD (show HSD17B10 Antibodies) is involved in thermogenesis, in the maintenance of body weight, and in the regulation of nutrient-stimulated insulin (show INS Antibodies) secretion
SCHAD (show HSD17B10 Antibodies) deficiency causes hyperinsulinism by activation of GDH (show UGDH Antibodies) via loss of inhibitory regulation of GDH (show UGDH Antibodies) by SCHAD (show HSD17B10 Antibodies).
Results demonstrate that L-3-hydroxyacyl-CoA dehydrogenase type II (show HSD17B10 Antibodies) (HADH (show HSD17B10 Antibodies) II/ABAD (show HSD17B10 Antibodies)) modulates 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity and suggests that mimetics may provide protective benefit in the treatment of Parkinson disease.
SCHAD (show HSD17B10 Antibodies) regulates insulin (show INS Antibodies) secretion through a KATP channel-independent mechanism.
This gene is a member of the 3-hydroxyacyl-CoA dehydrogenase gene family. The encoded protein functions in the mitochondrial matrix to catalyze the oxidation of straight-chain 3-hydroxyacyl-CoAs as part of the beta-oxidation pathway. Its enzymatic activity is highest with medium-chain-length fatty acids. Mutations in this gene cause one form of familial hyperinsulinemic hypoglycemia. The human genome contains a related pseudogene of this gene on chromosome 15.
hydroxyacyl-Coenzyme A dehydrogenase
, L-3-hydroxyacyl-Coenzyme A dehydrogenase
, L-3-hydroxyacyl-Coenzyme A dehydrogenase, short chain
, hydroxyacyl-coenzyme A dehydrogenase, mitochondrial
, 3-hydroxyacyl-CoA dehydrogenase (short-chain)
, Short chain 3-hydroxyacyl-CoA dehydrogenase
, short chain 3-hydroxyacyl-coa dehydrogenase
, medium and short-chain L-3-hydroxyacyl-coenzyme A dehydrogenase
, short-chain 3-hydroxyacyl-CoA dehydrogenase
, hydroxylacyl-Coenzyme A dehydrogenase short chain
, hydroxylacyl-Coenzyme A dehydrogenase, short chain
, medium and short chain L-3-hydroxyacyl-coenzyme A dehydrogenase
, short chain 3-hydroxyacyl-CoA dehydrogenase
, L-3-hydroxyacyl-CoA dehydrogenase
, hydroxylacyl-Coenzyme A dehydrogenase-dehydrogenase