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

Acetyl-CoA carboxylase beta

ACC2, ACCbeta, acetyl-CoA carboxylase 2
Acetyl-CoA carboxylase (ACC) is a complex multifunctional enzyme system. ACC is a biotin-containing enzyme which catalyzes the carboxylation of acetyl-CoA to malonyl-CoA, the rate-limiting step in fatty acid synthesis. ACC-beta is thought to control fatty acid oxidation by means of the ability of malonyl-CoA to inhibit carnitine-palmitoyl-CoA transferase I, the rate-limiting step in fatty acid uptake and oxidation by mitochondria. ACC-beta may be involved in the regulation of fatty acid oxidation, rather than fatty acid biosynthesis. There is evidence for the presence of two ACC-beta isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, AMPK, Insulin, HAD, CAN
Papers on ACC2
1,25-Dihydroxyvitamin D3 alleviates salivary adenoid cystic carcinoma progression by suppressing GPX1 expression through the NF-κB pathway.
Shen et al., Guangzhou, China. In Int J Oncol, Feb 2016
Pre-processing 1,25D3 inhibited expression of NF-κB/GPX1/uPA, which subsequently suppressed cell motility and cisplatin-resistance in ACC-2 cells.
Minimal impact of age and housing temperature on the metabolic phenotype of ACC2-/- mice.
Cooney et al., Sydney, Australia. In J Endocrinol, Jan 2016
UNASSIGNED: An important regulator of fatty acid oxidation (FAO) is the allosteric inhibition of CPT-1 by malonyl-CoA produced by the enzyme acetyl-CoA carboxylase 2 (ACC2).
Gut Microbial Fatty Acid Metabolites Reduce Triacylglycerol Levels in Hepatocytes.
Sugawara et al., Kyoto, Japan. In Lipids, Nov 2015
Oral administration of KetoA, which effectively reduced triacylglycerol accumulation and acetyl-CoA carboxylase 2 (ACC2) expression in HepG2 cells, for 2 weeks significantly decreased Srebp-1c, Scd-1, and Acc2 expression in the liver of mice fed a high-sucrose diet.
Effect of Creosote Bush-Derived NDGA on Expression of Genes Involved in Lipid Metabolism in Liver of High-Fructose Fed Rats: Relevance to NDGA Amelioration of Hypertriglyceridemia and Hepatic Steatosis.
Azhar et al., Palo Alto, United States. In Plos One, 2014
Western blot analysis indicated that NDGA administration upregulated hepatic insulin signaling (P-Akt), AMPK activity (P-AMPK), MLYCD, and PPARα protein levels, but decreased SCD1, ACC1 and ACC2 protein content and also inactivated ACC1 activity (increased P-ACC1).
Synthesis, Biological Evaluation and Molecular Docking Studies of Piperidinylpiperidines and Spirochromanones Possessing Quinoline Moieties as Acetyl-CoA Carboxylase Inhibitors.
Liu et al., Xuzhou, China. In Molecules, 2014
Most compounds showed moderate to good ACC inhibitory activities and compound 7a possessed the most potent biological activities against ACC1 and ACC2, with IC50 values of 189 nM and 172 nM, respectively, comparable to the positive control.
Aberrant Wnt-1/beta-catenin signaling and WIF-1 deficiency are important events which promote tumor cell invasion and metastasis in salivary gland adenoid cystic carcinoma.
Chen et al., Chengdu, China. In Biomed Mater Eng, 2014
Several sAdCC cell lines with low invasive potential (ACC-2), high metastatic potential (ACC-M), and higher invasive potential (T-ACC-M) were examined to determine whether Wnt components correlate with tumors' invasive and metastatic behavior.
Inhibition of acetyl-CoA carboxylase 2 enhances skeletal muscle fatty acid oxidation and improves whole-body glucose homeostasis in db/db mice.
Neubauer et al., Biberach an der Riß, Germany. In Diabetologia, 2012
Inhibition of acetyl-CoA carboxylase 2 enhances skeletal muscle fatty acid oxidation and improves whole-body glucose homeostasis in db/db mice.
AMPK regulates NADPH homeostasis to promote tumour cell survival during energy stress.
Hay et al., Chicago, United States. In Nature, 2012
The inhibition of the acetyl-CoA carboxylases ACC1 and ACC2 by AMPK maintains NADPH levels by decreasing NADPH consumption in fatty-acid synthesis and increasing NADPH generation by means of fatty-acid oxidation.
Acetyl-CoA carboxylase 2-/- mutant mice are protected against fatty liver under high-fat, high-carbohydrate dietary and de novo lipogenic conditions.
Wakil et al., Houston, United States. In J Biol Chem, 2012
the ACC2 deletion protects against fatty liver, despite increased de novo lipogenesis and a diet that induces obesity, fatty liver, and diabetes.
Structure-guided inhibitor design for human acetyl-coenzyme A carboxylase by interspecies active site conversion.
Vajdos et al., United States. In J Biol Chem, 2012
Structure-guided inhibitor design for human acetyl-coenzyme A carboxylase by interspecies active site conversion.
Association of ACACB polymorphisms with obesity and diabetes.
Rodríguez-Rey et al., Santander, Spain. In Mol Genet Metab, 2011
In conclusion, common polymorphisms of ACACB gene are associated with obesity and, independently, with type 2 diabetes in postmenopausal women
Deletion of the mammalian INDY homolog mimics aspects of dietary restriction and protects against adiposity and insulin resistance in mice.
Shulman et al., New Haven, United States. In Cell Metab, 2011
Deletion of mIndy in mice (mINDY(-/-) mice) reduces hepatocellular ATP/ADP ratio, activates hepatic AMPK, induces PGC-1α, inhibits ACC-2, and reduces SREBP-1c levels.
The effect of ACACB cis-variants on gene expression and metabolic traits.
Freedman et al., Winston-Salem, United States. In Plos One, 2010
Common variants within the ACACB locus appear to regulate adipose gene expression
Lipotoxicity in diabetic nephropathy: the potential role of fatty acid oxidation.
Ma et al., Winston-Salem, United States. In Clin J Am Soc Nephrol, 2010
The ACACB gene (also called ACC2 or acetyl-CoA carboxylase 2) plays a critical role in intracellular fatty acid (FA) oxidation.
Regulatory enzymes of mitochondrial beta-oxidation as targets for treatment of the metabolic syndrome.
van der Leij et al., Groningen, Netherlands. In Obes Rev, 2010
Evidence indicates that ACC2, the isoform located in close proximity to CPT1, is the major regulator of CPT1 activity.
Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity.
Cooney et al., Australia. In Cell Metab, 2010
Activation of AMP-activated protein kinase (AMPK) is thought to convey many of the beneficial effects of exercise via its inhibitory effect on acetyl-CoA carboxylase 2 (ACC2) and promotion of fatty acid oxidation.
Acetyl-CoA carboxylase-a as a novel target for cancer therapy.
Cao et al., Changsha, China. In Front Biosci (schol Ed), 2009
ACC-alpha (ACCA, also termed ACC1) and ACC-beta (ACCB, also designated ACC2).
Role of exercise-induced brain-derived neurotrophic factor production in the regulation of energy homeostasis in mammals.
Febbraio et al., Copenhagen, Denmark. In Exp Physiol, 2009
Brain-derived neurotrophic factor mRNA and protein expression was increased in muscle cells that were electrically stimulated, and BDNF increased phosphorylation of AMP-activated protein kinase (AMPK) and acetyl coenzyme A carboxylase-beta (ACCbeta) and enhanced fatty oxidation both in vitro and ex vivo.
Review of recent acetyl-CoA carboxylase inhibitor patents: mid-2007-2008.
Corbett, United States. In Expert Opin Ther Pat, 2009
CONCLUSION: These published patent applications include ACC inhibitors that inhibit the enzyme through modulation of the carboxyltransferase-domain, inhibitors that bind to the biotin carboxylase-domain and novel chemotypes whose mode of action was not disclosed.
Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2.
Wakil et al., Houston, United States. In Science, 2001
Malonyl-coenzyme A (malonyl-CoA), generated by acetyl-CoA carboxylases ACC1 and ACC2, is a key metabolite in the regulation of energy homeostasis.
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