anti-Sterol O-Acyltransferase 2 (SOAT2) 抗体

Human Sterol O-Acyltransferase 2 (SOAT2) interaction partners

1. 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.

2. ACAT-2 expression was negative in clear cell type renal cell carcinoma and normal kidney.

3. ACAT2 expression was induced upon R1881 (androgen agonist) treatment in prostate cancer cells

4. HNF4alpha positively regulates ACAT2 gene expression at mRNA level. Overexpression of HNF4alpha increased ACAT2 expression, whereas knockdown of HNF4alpha decreased ACAT2 expression.

5. 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

6. Low ACAT2 expression is associated with clear cell renal cell carcinoma.

7. 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

8. 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 lipid homeostasis.

9. human ACAT2 is transcriptionally regulated by cholesterol.

10. TG-interacting factor 1 (Tgif1) is an important repressor of SOAT2 gene expression.

11. CDX2, a known positive regulator of hepatocyte differentiation, was regulated by miR-181d and directly activated SOAT2 gene expression.

12. We found a new single-nucleotide polymorphism (SNP; a point mutation in intron 1, IVS1 -8 G-->C) in the ACAT-2 gene. Our data suggest that the ACAT-2 gene may not affect lipid levels in humans.

13. Fully differentiated macrophages express ACAT2 in addition to ACAT1 under various pathologic conditions.

14. ACAT-1 transcripts predominate in human liver and ACAT-2 transcripts predominate in human duodenum and support the notion that ACAT-2 has an important regulatory role in liver and intestine.

15. increasing DGAT1, ACAT1, or ACAT2 expression stimulates the assembly and secretion of VLDL from liver cells

16. ACAT2 provided the major cholesterol-esterifying activity in 3 of 4 human liver samples.

17. transcription factors hepatic nuclear factor 1 (HNF1)alpha and beta play an important part in the regulation of the ACAT2 promoter

18. The structural features of various sterols as substrates and/or activators of ACAT1 and ACAT2 in vitro are reported.

19. Serum-induced depletion of cellular cholesterol available for esterification by ACAT was a strong, independent predictor of major adverse cardiovascular events and death.

20. Elevated ACAT2 expression may serve as a new biomarker for certain form(s) of hepatocellular carcinoma.

Mouse (Murine) Sterol O-Acyltransferase 2 (SOAT2) interaction partners

1. ACAT2 provides core CE of newly secreted VLDL, whereas LCAT adds CE during LDL particle formation

2. ABCA1, especially in the absence of ACAT2, can have a significant effect on cholesterol absorption, although ACAT2 has a more substantial role in this process than ABCA1

3. depletion of hepatic ACAT2-driven cholesterol esterification reveals a non-biliary route for fecal neutral sterol loss

4. Inhibition of acyl-coenzyme A:cholesterol acyltransferase 2 prevents dietary cholesterol-associated steatosis by enhancing hepatic triglyceride mobilization.

5. Pyripyropene ACAT2-selective inhibition in the intestine and the liver can be effective against atherosclerosis.

6. inhibition of intestinal or hepatic ACAT2 improves atherogenic hyperlipidemia and limits hepatic cholesteryl ester accumulation

7. 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

8. ACAT2 seems to be a hepatic player affecting the cholesterol fluxes fated to VLDL or to HDL, the latter via up-regulation of ABCA1

9. Intestine-specific MTP and global ACAT2 deficiency lowers acute cholesterol absorption with chylomicrons and HDLs

10. 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 and fine-tuning lipid homeostasis.

11. These studies demonstrate that SOAT2 is a negative regulator of LXR-stimulated fecal neutral sterol loss in mice.

12. 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.

13. SOAT2 causes hepatic cholesterol to be swiftly mobilized and packaged onto nascent lipoproteins that feed cholesterol into the TICE pathway for fecal excretion.

14. effect the loss of SOAT2 function has on tissue esterified cholesterol sequestration in lysosomal acid lipase-deficient mice in a model of cholesteryl ester storage disease

15. Aortic atherosclerosis development was significantly lower in SOAT2 knock-out mice.

16. 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.

17. ACAT2-derived cholesterol esters have a crucial role in the development of atherosclerosis in mice

18. ACAT2 displays a greater capacity than ACAT1 to differentiate cholesterol from sitosterol

19. ACAT2-derived cholesteryl ester is the predominant atherogenic lipid in blood.

20. ACAT2 deficiency limits cholesterol absorption. Extent it impacts hepatic cholesterol homeostasis depends on cholesterol intake. Loss of ACAT2 activity may result in unesterified cholesterol being absorbed via ABCA1-mediated basolateral efflux pathway.

Zebrafish Sterol O-Acyltransferase 2 (SOAT2) interaction partners

1. These results indicated that zebrafish Soat2 is catalytically active in synthesizing cholesteryl esters and contributes to the yolk cholesterol trafficking during zebrafish embryogenesis.