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anti-Human HADH Antikörper:
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Human Monoclonal HADH Primary Antibody für 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 für 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 (zeige CYP Antikörper) member 8 (ABCC8 (zeige ABCC8 Antikörper)) gene, followed by 3-hydroxyacyl CoA dehydrogenase (HADH) and kcnj11 (zeige KCNJ11 Antikörper) channel (KCNJ11 (zeige KCNJ11 Antikörper)) genes.
We present clinical and laboratory findings together with the long-term clinical course of a case with a deep intronic HADH (zeige HADHA Antikörper) 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 (zeige HADHA Antikörper) mutations and 26% had ABCC8 (zeige ABCC8 Antikörper) mutations.
Next-generation sequencing reveals deep intronic cryptic ABCC8 (zeige ABCC8 Antikörper) and HADH (zeige HADHA Antikörper) 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 (zeige HADHA Antikörper) deficiency.
We recommend that HADH (zeige HADHA Antikörper) sequence analysis is considered in all patients with diazoxide-responsive hyperinsulinemic hypoglycemia when recessive inheritance is suspected
Congenital hyperinsulinism due to mutations in HNF4A (zeige HNF4A Antikörper) and HADH (zeige HADHA Antikörper).
SCHAD (zeige HSD17B10 Antikörper) 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 (zeige HSD17B10 Antikörper) is involved in thermogenesis, in the maintenance of body weight, and in the regulation of nutrient-stimulated insulin (zeige INS Antikörper) secretion
SCHAD (zeige HSD17B10 Antikörper) deficiency causes hyperinsulinism by activation of GDH (zeige UGDH Antikörper) via loss of inhibitory regulation of GDH (zeige UGDH Antikörper) by SCHAD (zeige HSD17B10 Antikörper).
Results demonstrate that L-3-hydroxyacyl-CoA dehydrogenase type II (zeige HSD17B10 Antikörper) (HADH (zeige HSD17B10 Antikörper) II/ABAD (zeige HSD17B10 Antikörper)) 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 (zeige HSD17B10 Antikörper) regulates insulin (zeige INS Antikörper) 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