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ACAT2 is a member of a small family of acyl coenzyme A:cholesterol acyltransferases. Zusätzlich bieten wir Ihnen ACAT2 Antikörper (106) und ACAT2 Proteine (15) und viele weitere Produktgruppen zu diesem Protein an.
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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 (zeige 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
TG-interacting factor 1 (Tgif1) is an important repressor of SOAT2 gene expression.
Results show that DLAT (zeige DLAT ELISA Kits) and ACAT2 as upstream acetyltransferases of K76 and K294 in 6PGD (zeige PGD ELISA Kits) protein.
CDX2, a known positive regulator of hepatocyte differentiation, was regulated by miR-181d and directly activated SOAT2 gene expression.
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.
lipid-induced stabilization of ACAT2 ameliorates lipotoxicity from excessive cholesterol and fatty acid. This unconventional cysteine ubiquitylation of ACAT2 constitutes an important mechanism for sensing lipid-overload-induced ROS (zeige ROS1 ELISA Kits) and fine-tuning lipid homeostasis.
These studies demonstrate that SOAT2 is a negative regulator of LXR-stimulated fecal neutral sterol loss in mice.
Hepatic knockdown of SOAT2 in apoB100-only, LDLr(-/-) mice resulted in remodeling of aortic atherosclerotic lesions into a stable phenotype, suggesting SOAT2 is a viable target for the treatment of atherosclerosis.
Intestine-specific MTP and global ACAT2 deficiency lowers acute cholesterol absorption with chylomicrons and HDLs (zeige CSF1R ELISA Kits)
SOAT2 causes hepatic cholesterol to be swiftly mobilized and packaged onto nascent lipoproteins that feed cholesterol into the TICE pathway for fecal excretion.
effect the loss of SOAT2 function has on tissue esterified cholesterol sequestration in lysosomal acid lipase (zeige LIPA ELISA Kits)-deficient mice in a model of cholesteryl ester storage disease
ACAT2 seems to be a hepatic player affecting the cholesterol fluxes fated to VLDL or to HDL (zeige HSD11B1 ELISA Kits), the latter via up-regulation of ABCA1 (zeige ABCA1 ELISA Kits)
Aortic atherosclerosis development was significantly lower in SOAT2 knock-out mice.
ACAT2 increases cholesterol absorption efficiency by providing cholesterol esters for chylomicron transport, but 1 copy of the Acat2 gene, providing approximately 50% of ACAT2 mRNA and enzyme activity, was as effective as 2 copies in promoting cholesterol absorption.
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
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 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