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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Hydroxyacyl-CoA dehydrogenase

HAD, 3-Hydroxyanthranilate 3,4-Dioxygenase, hydroxyacyl-coenzyme A dehydrogenase, Hao, HADH
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. [provided by RefSeq, May 2010] (from NCBI)
Top mentioned proteins: ACID, CAN, V1a, AGE, gp120
Papers on HAD
l-2-Haloacid dehalogenase from Ancylobacter aquaticus UV5: Sequence determination and structure prediction.
Olaniran et al., Durban, South Africa. In Int J Biol Macromol, Feb 2016
NCBI-BLAST of l-2-DhlB resulted in the detection of a putative conserved domain of hypothetical haloacid dehalogenase (HAD)-like superfamily and subfamily IA.
Clinical, genetic characteristics, management and long-term follow up of Turkish patients with congenital hyperinsulinism.
Flanagan et al., In J Clin Res Pediatr Endocrinol, Jan 2016
RESULTS: Seven infants were born large for gestational age, hypoglycemia was diagnosed within the first 24 hours of life in 9 patients and treatment with diazoxide (n=21) and/or somatostatin (n=8) had been attempted.
The Establishment and Characteristics of Rat Model of Atherosclerosis Induced by Hyperuricemia.
Li et al., Qingdao, China. In Stem Cells Int, Dec 2015
Wistar-Kyoto rats were randomly allocated to either a normal diet (ND), high-fat diet (HFD), or high-adenine diet (HAD), followed by sacrifice 4, 8, or 12 weeks later.
The extended human PTPome: A growing tyrosine phosphatase family.
Pulido et al., Valladolid, Spain. In Febs J, Dec 2015
This activity is found in several structurally diverse protein families, including Protein Tyrosine Phosphatase (PTP), Arsenate Reductase, Rhodanese, Haloacid Dehalogenase (HAD), and Histidine Phosphatase (HP) families.
Uncovering the molecular pathogenesis of congenital hyperinsulinism by panel gene sequencing in 32 Chinese patients.
Zhou et al., Shanghai, China. In Mol Genet Genomic Med, Nov 2015
Four patients had mutations in KCNJ11, 1 had a GCK mutation, 1 had a mutation in HADH, and two had a mutation in HNF4A.
A comparative study of dried apple using hot air, intermittent and continuous microwave: evaluation of kinetic parameters and physicochemical quality attributes.
Maleki et al., Karaj, Iran. In Food Sci Nutr, Nov 2015
In the study, the effectiveness of intermittent (IMWD) and continuous (CMWD) microwave drying and hot air drying (HAD) treatments on apple slices were compared in terms of drying kinetics (moisture diffusivity and activation energy) and critical physicochemical quality attributes (color change, rehydration ratio, bulk density, and total phenol content (TPC) of the final dried product.
Molecular mechanisms of congenital hyperinsulinism.
Hussain et al., London, United Kingdom. In J Mol Endocrinol, Apr 2015
Mutations in GLUD1 and HADH lead to leucine-induced HH, and these two genes encode the key enzymes glutamate dehydrogenase and short chain 3-hydroxyacyl-CoA dehydrogenase which play a key role in amino acid and fatty acid regulation of insulin secretion respectively.
Current gene therapy using viral vectors for chronic pain.
Hao et al., Pittsburgh, United States. In Mol Pain, 2014
Dr. Hao group addresses the observation that the pro-inflammatory cytokines are an important shared mechanism underlying both neuropathic pain and the development of opioid analgesic tolerance and withdrawal.
Neuropathogenesis of HIV-associated neurocognitive disorders: roles for immune activation, HIV blipping and viral tropism.
Kolson et al., Philadelphia, United States. In Curr Opin Hiv Aids, 2014
Prior to ART, HIV-associated dementia (HAD), the severest form of HAND, affected nearly 20% of infected individuals; HAD now affects only nearly 2% of ART-treated persons, although less severe HAND forms persist.
Molecular mechanisms of protein induced hyperinsulinaemic hypoglycaemia.
Hussain et al., Singapore, Singapore. In World J Diabetes, 2014
The observation of protein induced hypoglycaemia in patients with mutations in GLUD1 gene, encoding the enzyme glutamate dehydrogenase (GDH) and HADH gene, encoding for the enzyme short-chain 3-hydroxyacyl-CoA dehydrogenase has provided new mechanistic insights into the regulation of insulin secretion by amino acid and fatty acid metabolism.
Connecting with an old partner in a new way.
Williams et al., Cambridge, United Kingdom. In Cancer Cell, 2013
In this issue of Cancer Cell, Hao and colleagues report a non-canonical interaction between the insulin receptor substrate 1 and certain oncogenic variants of the p110α catalytic subunit of phosphoinositide 3-kinase (PI3K).
Small RNA-mediated activation of sugar phosphatase mRNA regulates glucose homeostasis.
Vogel et al., Würzburg, Germany. In Cell, 2013
Here, we identify the conserved haloacid dehalogenase (HAD)-like enzyme YigL as the previously hypothesized phosphatase for detoxification of phosphosugars and reveal that its synthesis is activated by an Hfq-dependent small RNA in Salmonella typhimurium.
Role of medium- and short-chain L-3-hydroxyacyl-CoA dehydrogenase in the regulation of body weight and thermogenesis.
Schürmann et al., Potsdam, Germany. In Endocrinology, 2011
SCHAD is involved in thermogenesis, in the maintenance of body weight, and in the regulation of nutrient-stimulated insulin secretion
Short-chain 3-hydroxyacyl-coenzyme A dehydrogenase associates with a protein super-complex integrating multiple metabolic pathways.
Bennett et al., Philadelphia, United States. In Plos One, 2011
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.
Short-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: the clinical relevance of an early diagnosis and report of four new cases.
Vilarinho et al., Porto, Portugal. In J Inherit Metab Dis, 2011
Clinical, biochemical and molecular findings of four new Caucasian patients with HADH deficiency.
Genome-wide homozygosity analysis reveals HADH mutations as a common cause of diazoxide-responsive hyperinsulinemic-hypoglycemia in consanguineous pedigrees.
Ellard et al., Exeter, United Kingdom. In J Clin Endocrinol Metab, 2011
We recommend that HADH sequence analysis is considered in all patients with diazoxide-responsive hyperinsulinemic hypoglycemia when recessive inheritance is suspected
Congenital hyperinsulinism due to mutations in HNF4A and HADH.
Hussain et al., London, United Kingdom. In Rev Endocr Metab Disord, 2010
Congenital hyperinsulinism due to mutations in HNF4A and HADH.
Regulation of cellular metabolism by protein lysine acetylation.
Guan et al., Shanghai, China. In Science, 2010
Acetylation activated enoyl-coenzyme A hydratase/3-hydroxyacyl-coenzyme A dehydrogenase in fatty acid oxidation and malate dehydrogenase in the TCA cycle, inhibited argininosuccinate lyase in the urea cycle, and destabilized phosphoenolpyruvate carboxykinase in gluconeogenesis.
HIV/gp120 decreases adult neural progenitor cell proliferation via checkpoint kinase-mediated cell-cycle withdrawal and G1 arrest.
Lipton et al., Los Angeles, United States. In Cell Stem Cell, 2007
Impaired adult neurogenesis has been observed in several neurodegenerative diseases, including human immunodeficiency virus (HIV-1)-associated dementia (HAD).
The neuropathogenesis of AIDS.
Martín-García et al., Philadelphia, United States. In Nat Rev Immunol, 2005
HIV-associated dementia (HAD) is an important complication of the central nervous system in patients who are infected with HIV-1.
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