carboxylase


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carboxylase

[kär′bäk·sə‚lās]
(biochemistry)
Any enzyme that catalyzes a carboxylation or decarboxylation reaction.
References in periodicals archive ?
Diagnosis###Molybdenum cofactor deficiency###Pyruvate carboxylase deficiency###Zellweger syndrome###Non-ketotichyperglycinemia
Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation.
Topical agents that release nitric oxide locally or target sebum by inhibiting acetyl coenzyme-A carboxylase, as well as a topical antiandrogen are in clinical trials.
Examples are individuals with metabolic disorders like pyruvate carboxylase deficiency, porphyria and other fat metabolism disorders.
Carboxylase, protease, lipase, polymerase and xylanase are major enzyme types majorly incorporated in formulation of baked products to improve organoleptic properties and crust appearance.
The researchers discovered a novel variant of phosphoenolpyruvate carboxylase, or PEPC.
The first step of fatty acid biosynthesis is the conversion of acetyl-CoA to malonyl-CoA, catalyzed by acetyl coenzyme A carboxylase (ACC).
Thyroid hormone has major effects on lipid metabolism by activating hepatic and AT lipogenesis via induction of enzymes involved in fatty acid synthesis, including acetyl CoA carboxylase (ACC) and fatty acid synthase (FASN) [13], increasing fatty acid [beta]-oxidation though carnitine palmitoyl transferase (CPT) [14,15], and enhancing lipolysis in animal models [16].
AMPK activates energy-generating pathways by increasing fatty acid oxidation via phosphorylation of acetyl-coA carboxylase 2 (ACC2) and glycolysis via activation of phosphofructo-2kinase (PFK) (Figure 1(a)).
At a molecular level, chronic exposition to fructose induce an upregulation of sterol regulatory element binding protein-1 (SREBP-1c) and the enzyme acetyl-coenzyme A carboxylase that can lead to increase of fat synthesis and hyperuricemia by high degradation of AMP and depletion of ATP content in the liver, all caused by the excessive synthesis of fructose-1-phosphate, a consequence of the excessive incorporation of fructose into blood circulation [8] which adds to liver inhibitions of NRF-2 (antioxidant transcription factor and liver steatosis inhibitor) and PGC1[alpha] expression [22] and stimulation of gluconeogenesis via FOXO1 and PEPCK expression [23].
Quizalofop-resistant rice is a non-GMO crop and was developed using traditional plant breeding techniques to isolate the G2096S gene, which makes the acetyl coenzyme A carboxylase enzyme resistant to ACCase-inhibiting herbicides [15].
Lawitz, MD, reported the promising results of a "proof of concept" open-label study in which the safety and efficacy of 12 weeks' treatment with the oral acetyl-CoA carboxylase (ACC) inhibitor, GS-0976, was examined in 10 patients with a clinical diagnosis of nonalcoholic fatty liver disease (NAFLD).