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anti-Human ACADL Anticorps:
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Human Polyclonal ACADL Primary Antibody pour ELISA, WB - ABIN559742
Tucci, Herebian, Sturm, Seibt, Spiekerkoetter: Tissue-specific strategies of the very-long chain acyl-CoA dehydrogenase-deficient (VLCAD-/-) mouse to compensate a defective fatty acid ?-oxidation. dans PLoS ONE 2012
Cow (Bovine) Polyclonal ACADL Primary Antibody pour WB - ABIN2778159
Lea, Abbas, Sprecher, Vockley, Schulz: Long-chain acyl-CoA dehydrogenase is a key enzyme in the mitochondrial beta-oxidation of unsaturated fatty acids. dans Biochimica et biophysica acta 2000
Show all 2 Pubmed References
Human Polyclonal ACADL Primary Antibody pour IHC (p), WB - ABIN652476
Geillinger, Rathmann, Köhrle, Fiamoncini, Daniel, Kipp: Hepatic metabolite profiles in mice with a suboptimal selenium status. dans The Journal of nutritional biochemistry 2014
the fatty acid oxidation pathway and LCAD are factors contributing to the pathophysiology of pulmonary disease
Sirtuin 3 (SIRT3 (Montrer SIRT3 Anticorps)) protein regulates long-chain acyl-CoA dehydrogenase by deacetylating conserved lysines near the active site.
LCAD is minimally expressed in human skeletal muscle and likely does not play a significant role in long-chain fatty acid oxidation.
LCAD-/- mice succumb to influenza from bioenergetic starvation, likely due to increased reliance upon glucose for energy.
SIRT3 (Montrer SIRT3 Anticorps) may play an essential role in attenuating lipid accumulation in the heart through the deacetylation of LCAD
Carnitine supplementation lowered myocardial triglycerides, normalizing myocardial triglycerides levels in LCAD Knock-out mice.
LCAD KO mice are ineffective in maintaining metabolic homeostasis during fasting, which is reflected by an impaired myocardial energy status in fasted LCAD KO mice.
mice with an inherited deficiency of very long-chain acyl-CoA dehydrogenase (VLCAD (Montrer ACADVL Anticorps)), were protected from high-fat diet-induced obesity and liver and muscle insulin (Montrer INS Anticorps) resistance.
LCAD is deacetylated in wild-type mice under fasted conditions and by SIRT3 (Montrer SIRT3 Anticorps) in vitro and in vivo; hyperacetylation of LCAD reduces its enzymatic activity
These data demonstrate that primary defects in mitochondrial fatty acid oxidation capacity can lead to diacylglycerol accumulation, PKCepsilon (Montrer PRKCE Anticorps) activation, and hepatic insulin (Montrer INS Anticorps) resistance.
Novel candidate genes in T1D CD55 (Montrer CD55 Anticorps) and Acadl were identified.
The protein encoded by this gene belongs to the acyl-CoA dehydrogenase family, which is a family of mitochondrial flavoenzymes involved in fatty acid and branched chain amino-acid metabolism. This protein is one of the four enzymes that catalyze the initial step of mitochondrial beta-oxidation of straight-chain fatty acid. Defects in this gene are the cause of long-chain acyl-CoA dehydrogenase (LCAD) deficiency, leading to nonketotic hypoglycemia.
, long-chain specific acyl-CoA dehydrogenase, mitochondrial
, acyl-Coenzyme A dehydrogenase, long chain
, long-chain acyl-CoA dehydrogenase
, Acyl Coenzyme A dehydrogenase, long chain
, LCAD long chain acyl-CoA dehydrogenase
, acetyl-Coenzyme A dehydrogenase, long-chain
, acyl-Coenzyme A dehydrogenase, long-chain