gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Acyl-CoA dehydrogenase, C-4 to C-12 straight chain

MCAD, medium-chain acyl-CoA dehydrogenase
This gene encodes the medium-chain specific (C4 to C12 straight chain) acyl-Coenzyme A dehydrogenase. The homotetramer enzyme catalyzes the initial step of the mitochondrial fatty acid beta-oxidation pathway. Defects in this gene cause medium-chain acyl-CoA dehydrogenase deficiency, a disease characterized by hepatic dysfunction, fasting hypoglycemia, and encephalopathy, which can result in infantile death. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, fibrillin-1, CAN, HAD, PPAR
Papers using MCAD antibodies
ATPase and phosphatase activity of Na+-K+-ATPase: Molar and specific activity, protein determination
Oyekan Adebayo O et al., In BMC Pharmacology, 1987
... Antibody to MCAD (medium chain acyldehydrogenase) and 1H-[1,2,4] oxadiazolo [4,3-α] quinoxalin-1-one (ODQ) were obtained from Cayman (Cayman Chemicals, Ann Arbor, ...
Papers on MCAD
Cardiovascular symptoms in patients with systemic mast cell activation disease.
Molderings et al., Bonn, Germany. In Transl Res, Jan 2016
UNASSIGNED: Traditionally, mast cell activation disease (MCAD) has been considered as just one rare (neoplastic) disease, mastocytosis, focused on the mast cell (MC) mediators tryptase and histamine and the suggestive, blatant symptoms of flushing and anaphylaxis.
Inborn Errors of Metabolism in the United Arab Emirates: Disorders Detected by Newborn Screening (2011-2014).
Souid et al., Al `Ayn, United Arab Emirates. In Jimd Rep, Dec 2015
The following eight disorders accounted for 80% of the entities: biotinidase deficiency (14 of 55), phenylketonuria (11 of 55), 3-methylcrotonyl glycinuria (9 of 55), medium-chain acyl-CoA dehydrogenase deficiency (4 of 55), argininosuccinic aciduria, glutaric aciduria type 1, glutaric aciduria type 2, and methylmalonyl-CoA mutase deficiency (2 of 55 each).
Mast cell activation disease: An underappreciated cause of neurologic and psychiatric symptoms and diseases.
Molderings et al., Minneapolis, United States. In Brain Behav Immun, Nov 2015
Systemic mast cell activation disease (MCAD) has rarely been considered in the differential diagnosis in such situations.
Amelioration of palmitate-induced metabolic dysfunction in L6 muscle cells expressing low levels of receptor-interacting protein 140.
Turcotte et al., Rancho Palos Verdes, United States. In Can J Physiol Pharmacol, Nov 2015
Under insulin-treated conditions, low RIP140 expression increased the mRNA content of MCAD (84%) and Nur77 (84%), as well as the protein content of Nur77 (23%).
FSH and bFGF regulate the expression of genes involved in Sertoli cell energetic metabolism.
Meroni et al., Buenos Aires, Argentina. In Gen Comp Endocrinol, Nov 2015
The expression of genes involved in transport and metabolism of FA such as: fatty acid transporter CD36 (FAT/CD36), carnitine-palmitoyltransferase 1 (CPT1), long- and medium-chain 3-hydroxyacyl-CoA dehydrogenases (LCAD, MCAD), and of genes involved in mitochondrial biogenesis such as: nuclear respiratory factors 1 and 2 (NRF1, NRF2) and transcription factor A (Tfam), was analyzed.
Resveratrol prevents renal lipotoxicity in high-fat diet-treated mouse model through regulating PPAR-α pathway.
Li et al., Wenzhou, China. In Mol Cell Biochem, Oct 2015
Mechanistically, RSV enhanced the expression of lipolytic genes, peroxisome proliferator-activated receptor (PPAR)-α (p < 0.001), carnitine palmitoyltransferase (CPT)-1 (p < 0.05), and medium-chain acyl-coenzyme A dehydrogenase (MCAD) (p < 0.01), but had no effect on lipogenic genes, PPAR-γ and sterol regulatory element-binding protein (SREBP)-1c.
Role of adenosine 5'-monophosphate-activated protein kinase in α-linolenic acid-induced intestinal lipid metabolism.
Wang et al., Hangzhou, China. In Br J Nutr, Oct 2015
ALA also increased mRNA expression of genes (carnitine palmitoyltransferase 1a, acyl-CoA oxidase 1, medium-chain acyl-CoA dehydrogenase, cytochrome P450 4A10 and pyruvate dehydrogenase kinase isoenzyme 4a) involved in intestinal lipid oxidation and mRNA expression of TAG synthesis-related genes (monoacylglycerol O-acyltransferase 2, diacylglycerol O-acyltransferases 1 and 2) in WT mice.
Mast Cell Activation Disease and Microbiotic Interactions.
Khoruts et al., Minneapolis, United States. In Clin Ther, Jun 2015
PURPOSE: This article reviews the diagnostically challenging presentation of mast cell activation disease (MCAD) and current thoughts regarding interactions between microbiota and MCs.
The genetic basis of mast cell activation disease - looking through a glass darkly.
Molderings, Bonn, Germany. In Crit Rev Oncol Hematol, Feb 2015
Within the last decade, and in particular since 2012, research has greatly extended our understanding of the molecular basis of systemic mast cell activation disease (MCAD).
FABP4 reversed the regulation of leptin on mitochondrial fatty acid oxidation in mice adipocytes.
Sun et al., China. In Sci Rep, 2014
Moreover, mitochondrial membrane potential, fatty acid oxidation enzyme medium-chain acyl-CoA dehydrogenase (MCAD), long-chain acyl-CoA dehydrogenase (LCAD) and Cyt C levels were reduced in response to the overexpression of FABP4.
Mitochondrial dysfunction in fatty acid oxidation disorders: insights from human and animal studies.
Amaral et al., Porto Alegre, Brazil. In Biosci Rep, 2014
We will briefly summarize the current knowledge obtained from patients and genetic mouse models with these disorders indicating that disruption of mitochondrial energy, redox and calcium homoeostasis is involved in the pathophysiology of the tissue damage in the more common FAOD, including medium-chain acyl-CoA dehydrogenase (MCAD), long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and very long-chain acyl-CoA dehydrogenase (VLCAD) deficiencies.
Cofactors and metabolites as potential stabilizers of mitochondrial acyl-CoA dehydrogenases.
Gomes et al., Lisbon, Portugal. In Biochim Biophys Acta, 2011
physiological concentrations of flavin adenine dinucleotide resulted in a spectacular enhancement of the thermal stabilities of MCADH and prevented enzymatic activity loss
Interactions between the consumption of a high-fat diet and fasting in the regulation of fatty acid oxidation enzyme gene expression: an evaluation of potential mechanisms.
Wright et al., Edmonton, Canada. In Am J Physiol Regul Integr Comp Physiol, 2011
High fat diets increase the expression of fatty acid oxidation enzymes such as UCP3,PDK4, and MCAD concomitant with elevated plasma fatty acid levels and the induction of PGC-1 beta, but independent of changes in AMPK, p38, and PKA signaling.
Clinical, biochemical and genetic analyses in two Korean patients with medium-chain acyl-CoA dehydrogenase deficiency.
Kim et al., Seoul, South Korea. In Korean J Lab Med, 2011
The mutation in Medium-chain acyl-CoA dehydrogenase deficiency is the first report of the c.461T>G mutation in the acyl-CoA dehydrogenase gene.
Allelic diversity in MCAD deficiency: the biochemical classification of 54 variants identified during 5 years of ACADM sequencing.
Oglesbee et al., Rochester, United States. In Mol Genet Metab, 2010
classification of genotypes with at least one variant of unknown significance in individuals who are carriers of, or affected with, MCAD deficiency of the following genotypes: c.985A>G/wildtype, c.199T>C/c.985A>G and c.985A>G/c.985A>G
A high-fat diet increases adiposity but maintains mitochondrial oxidative enzymes without affecting development of heart failure with pressure overload.
Stanley et al., Baltimore, United States. In Am J Physiol Heart Circ Physiol, 2009
A high-fat diet increases adiposity but maintains mitochondrial oxidative enzymes (MCAD/citrate synthase) without affecting development of heart failure with pressure overload.
Outcome of neonatal screening for medium-chain acyl-CoA dehydrogenase deficiency in Australia: a cohort study.
Boneh et al., Sydney, Australia. In Lancet, 2007
BACKGROUND: Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is the disorder thought most to justify neonatal screening by tandem-mass spectrometry because, without screening, there seems to be substantial morbidity and mortality.
Neonatal screening for medium-chain acyl-CoA dehydrogenase deficiency.
Bartlett et al., In Lancet, 2001
Neonatal screening for medium-chain acyl-CoA dehydrogenase (MCAD) deficiency has not yet been introduced in the UK, primarily because of uncertainty about the natural history of the disorder and concerns about the specificity of the screening test.
Prevalence of K329E mutation in medium-chain acyl-CoA dehydrogenase gene determined from Guthrie cards.
McCabe et al., Japan. In Lancet, 1991
Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is an autosomal recessive disorder that has been associated with sudden infant death syndrome and a condition resembling Reye's syndrome.
Dicarboxylic aciduria: deficient [1-14C]octanoate oxidation and medium-chain acyl-CoA dehydrogenase in fibroblasts.
Felts et al., In Science, 1983
Dicarboxylic aciduria, an inborn error of metabolism in man, is thought to be caused by defective beta-oxidation of six-carbon to ten-carbon fatty acids.
share on facebooktweetadd +1mail to friends