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The product of ACAT2 is an enzyme involved in lipid metabolism, and it encodes cytosolic acetoacetyl-CoA thiolase. Additionally we are shipping ACAT2 Antibodies (107) and ACAT2 Proteins (15) and many more products for this protein.
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Lipid-induced stabilization of ACAT2 ameliorates lipotoxicity from excessive cholesterol and fatty acid. Cysteine ubiquitylation of ACAT2 constitutes an important mechanism for sensing lipid-overload-induced ROS and fine-tuning lip (show ROS1 ELISA Kits)id homeostasis.
data demonstrate that the ACAT2 expression of human leukocytes is responsible for the excretion of lipoproteins containing cholesteryl/steryl esters (CE/SE), and suggest that the excretion of lipoproteins containing the ACAT2-catalyzed CS/SE may avoid cytotoxicity
results demonstrate that the low-level expression of human ACAT2 gene with specific CpG-hypomethylated promoter is regulated by the C/EBP transcription factors in monocytic cells, and imply that the lowly expressed ACAT2 catalyzes the synthesis of certain CE/SE that are assembled into lipoproteins for the secretion
Low ACAT2 expression is associated with clear cell renal cell carcinoma.
results show that the enzymatic activity of mutant Glu(14)Gly is approximately two times higher than wildtype, and that this increase is primarily due to the increased expression and/or stability of the mutant ACAT2 protein
Results show that DLAT (show DLAT ELISA Kits) and ACAT2 as upstream acetyltransferases of K76 and K294 in 6PGD (show PGD ELISA Kits) protein.
Reduced ACAT2 is associated with impaired butyrate oxidation in ulcerative colitis.
HNF4alpha positively regulates ACAT2 gene expression at mRNA level. Overexpression of HNF4alpha increased ACAT2 expression, whereas knockdown of HNF4alpha decreased ACAT2 expression.
Describe a gender-related difference in hepatic ACAT2 activity in normolipidemic non-obese Chinese patients suggesting a possible role for ACAT2 in the regulation of cholesterol metabolism in humans.
Data describe the high resolution structure of human cytosolic acetoacetyl-CoA thiolase (CT), both unliganded (at 2.3 angstroms resolution) and in complex with CoA (at 1.6 angstroms resolution).
lipid-induced stabilization of ACAT2 (show SOAT2 ELISA Kits) ameliorates lipotoxicity from excessive cholesterol and fatty acid. This unconventional cysteine ubiquitylation of ACAT2 (show SOAT2 ELISA Kits) constitutes an important mechanism for sensing lipid-overload-induced ROS (show ROS1 ELISA Kits) and fine-tuning lipid homeostasis.
Intestine-specific MTP (show LAPTM4A ELISA Kits) and global ACAT2 (show SOAT2 ELISA Kits) deficiency lowers acute cholesterol absorption with chylomicrons and HDLs (show CSF1R ELISA Kits)
ACAT2 (show SOAT2 ELISA Kits) seems to be a hepatic player affecting the cholesterol fluxes fated to VLDL or to HDL (show HSD11B1 ELISA Kits), the latter via up-regulation of ABCA1 (show ABCA1 ELISA Kits)
handling of sterols by the intestine involves both G5G8 and ACAT2 but that an additional factor (possibly Niemann-Pick C1-like 1) may be key in determining absorption efficiency
inhibition of intestinal or hepatic ACAT2 improves atherogenic hyperlipidemia and limits hepatic cholesteryl ester accumulation
Pyripyropene ACAT2-selective inhibition in the intestine and the liver can be effective against atherosclerosis.
Inhibition of acyl-coenzyme A:cholesterol acyltransferase 2 (show SOAT2 ELISA Kits) prevents dietary cholesterol-associated steatosis by enhancing hepatic triglyceride mobilization.
ACAT2 (show SOAT2 ELISA Kits) provides core CE of newly secreted VLDL, whereas LCAT (show LCAT ELISA Kits) adds CE during LDL particle formation
ABCA1 (show ABCA1 ELISA Kits), especially in the absence of ACAT2 (show SOAT2 ELISA Kits), can have a significant effect on cholesterol absorption, although ACAT2 (show SOAT2 ELISA Kits) has a more substantial role in this process than ABCA1 (show ABCA1 ELISA Kits)
depletion of hepatic ACAT2-driven cholesterol esterification reveals a non-biliary route for fecal neutral sterol loss
The AACT2-derived acetoacetyl CoA pool generates isoprenoids that are required for normal growth and development. AACT2 is essential and cannot be replaced by AACT1. AACT1 and AACT2 exhibit differential spatial and temporal expression patterns.
ACAT2 might contribute more to metabolic processes than ACAA2 (show ACAA2 ELISA Kits) in swine.
The product of this gene is an enzyme involved in lipid metabolism, and it encodes cytosolic acetoacetyl-CoA thiolase. This gene shows complementary overlapping with the 3-prime region of the TCP1 gene in both mouse and human. These genes are encoded on opposite strands of DNA, as well as in opposite transcriptional orientation.
acetoacetyl Coenzyme A thiolase
, acetyl-CoA acetyltransferase, cytosolic
, acetyl-CoA transferase-like protein
, cytosolic acetoacetyl-CoA thiolase
, acetyl-Coenzyme A acyltransferase 2
, t-complex protein 1, related sequence 1
, acetyl-Coenzyme A acetyltransferase 2
, acetyl-Coenzyme A acetyltransferase 3
, acetyl-Coenzyme A acetyltransferase 2 (acetoacetyl Coenzyme A thiolase)
, acetyl-CoA acetyltransferase 2
, acetyl-CoA acetyltransferase, cytosolic-like