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anti-Human Acetyl-CoA Carboxylase alpha Antibodies:
anti-Rat (Rattus) Acetyl-CoA Carboxylase alpha Antibodies:
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sensitive to freezing3(sfr3) is a missense mutation in aminoglycoside N1-acetyltransferase. Freezing sensitivity of sfr3 appears to be due to cuticular deficiencies that develop during cold acclimation.
The gsd1 (show G6PC Antibodies) locus was mapped to chromosome 1, and the causal gene was identified as a new allele of Acetyl-Coenzyme A Carboxylase1 (ACC1), a gene encoding the main enzyme in cytosolic malonyl-coenzyme A synthesis.
Data suggest that the lack of cytosolic malonyl-CoA is likely to be the initial factor leading to abnormal development in acetyl-CoA carboxylase 1 mutants.
the present studies report for the first time a role of ACC1 in suppressing breast cancer migration and invasion by an fatty acid synthesis-independent, but acetyl-CoA (show LPCAT2 Antibodies)-dependent, impact on the epithelial-mesenchymal transition programs in breast tumor cells and its subsequent importance for tumor invasion and recurrence.
the presence of an internal ribosome entry site in the ACC1 5' UTR (show UTS2R Antibodies) allows ACC1 mRNA translation in conditions that are inhibitory to cap-dependent translation.
of ACCs decreased polyunsaturated fatty acid (PUFA) concentrations in liver due to reduced malonyl-CoA, which is required for elongation of essential fatty acids.
Inhibition of Acetyl-CoA Carboxylase 1 (ACC1) and 2 (ACC2 (show ACACB Antibodies)) Reduces Proliferation and De Novo Lipogenesis of EGFRvIII Human Glioblastoma Cells
Cetuximab-mediated activation of AMPK and subsequent phosphorylation and inhibition of ACC is followed by a compensatory increase in total ACC, which rewires cancer metabolism from glycolysis-dependent to lipogenesis-dependent.
acetyl-CoA carboxylase 1 and senescence regulation in human fibroblasts involves oxidant mediated p38 MAPK (show MAPK14 Antibodies) activation
ACC1 and ACLY (show ACLY Antibodies) regulate the levels of ETV4 (show ETV4 Antibodies) under hypoxia via increased alpha-ketoglutarate. These results reveal that the ACC1/ACLY (show ACLY Antibodies)-alpha-ketoglutarate-ETV4 (show ETV4 Antibodies) axis is a novel means by which metabolic states regulate transcriptional output
Phospho-acetyl-CoA carboxylase protein expression correlates with tumor grade and the disease stage in gastric cancer.
ACAT1 (show ACAT1 Antibodies), ACACA, ALDH6A1 (show ALDH6A1 Antibodies) and MTHFD1 (show MTHFD1 Antibodies) represent novel biomarkers in adipose tissue associated with type 2 diabetes in obese individuals.
ACACA may constitute a previously unrecognized target for novel anti-breast cancer stem cell therapies.
Polymorphisms of the ACACA and SREBF1 (show SREBF1 Antibodies) genes are promising markers for pig carcass and performance traits.
Expression profiles showed that PI is the promoter driving expression of the dominant ACACA-transcript in brain.
Since the promoter region, PIII, is specific to mammary gland during lactation, the altered expression of the ACACA gene owing to the SNPs in the PIII region may influence the fatty acid composition in the milk.
results suggested that the SNPs in the promoter I region of ACACA gene are associated with variations in the fatty acid contents in longissimus dorsi muscle.
the present studies report for the first time a role of ACC1 in suppressing breast cancer migration and invasion by an fatty acid synthesis-independent, but acetyl-CoA (show LPCAT1 Antibodies)-dependent, impact on the epithelial-mesenchymal transition programs in breast tumor cells and its subsequent importance for tumor invasion and recurrence.
madecassic acid was the active form of madecassoside in ameliorating colitis by restoring the Th17/Treg balance via regulating the PPARgamma (show PPARG Antibodies)/AMPK (show PRKAA1 Antibodies)/ACC1 pathway.
Studied a role for ACAC inactivation in meiotic resumption by testing the effect of two ACAC inhibitors, CP-640186 and Soraphen A, on mouse oocytes maintained in meiotic arrest in vitro.
AMPK (show PRKAA1 Antibodies)-dependent inactivation of ACC is not essential for the control of myocardial FAO and subsequent cardiac function during a variety of conditions involving AMPK (show PRKAA1 Antibodies)-independent and AMPK (show PRKAA1 Antibodies)-dependent metabolic adaptations.
Results suggest an essential role for acetyl coenzyme A carboxylase 1 (ACC1)-mediated de novo lipogenesis as a regulator of CD8 (show CD8A Antibodies)(+) T cell expansion.
the stimulation of fatty acid oxidation by modulating the AMPK (show PRKAA1 Antibodies)-ACC-CPT-1 (show CPT1A Antibodies) pathway may be part of a protective mechanism against saturated free fatty acids that drive podocyte death.
our data suggest that renin (show REN Antibodies) synthesis and secretion are regulated by AMPK (show PRKAA1 Antibodies) and coupled to metabolism by phosphorylation of ACC1.
analysis of mRNA abundance and expression of SLC27A, ACC, SCD, FADS, LPIN, INSIG, and PPARGC1 gene isoforms in mouse mammary glands during the lactation cycle
A biotin analog inhibits acetyl-CoA carboxylase activity and adipogenesis
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. There are two ACC forms, alpha and beta, encoded by two different genes. ACC-alpha is highly enriched in lipogenic tissues. The enzyme is under long term control at the transcriptional and translational levels and under short term regulation by the phosphorylation/dephosphorylation of targeted serine residues and by allosteric transformation by citrate or palmitoyl-CoA. Multiple alternatively spliced transcript variants divergent in the 5' sequence and encoding distinct isoforms have been found for this gene.
acetyl-Coenzyme A carboxylase alpha
, acetyl-CoA carboxylase 1
, acetyl-coenzyme A carboxylase alpha
, acetyl-CoA carboxylase-alpha
, acetyl-CoA carboxylase
, acetyl coenzyme A carboxylase alpha
, acetyl-CoA carboxylase 265