Sterol O-Acyltransferase 1 (SOAT1) Kits ELISA

Human Sterol O-Acyltransferase 1 (SOAT1) interaction partners

1. There was a significant difference and a higher frequency of AA and AC genotypes (p = 0.047 and p = 0.016, respectively) of the SOAT1 (ACAT-1) gene in asymptomatic chagasic individuals.

2. the transcription factor signal transducer and activator of transcription 3 was activated by TB-PE, and its chemical inhibition prevented the accumulation of lipid bodies and ACAT expression in macrophages. In terms of the host immune response, TB-PE-treated macrophages displayed immunosuppressive properties and bore higher bacillary loads.

3. Soat-1 role in atherosclerosis

4. Several residues in one subunit closely interact with the same residues in the other subunit; mutating these res. to Cys does not lead to loss in enzyme activity. Mutating residues F453, A457, or H460 to Cys causes large loss in enzyme activity.

5. increase in the in vitro ACAT1 activity in PC-3 prostate cancer cells treated with androgen

6. The results suggest that rs1044925 polymorphism in ACAT1 gene is not only associated with serum LDL-C and nHDLC levels in healthy Chinese subjects in Chengdu area, but also with HDL-C level in subjects with endogenous hypertriglyceridemia.

7. RNA secondary structures located in the vicinity of the GGC(1274-1276) codon are required for production of the 56-kDa isoform.

8. ACAT inhibition may stimulate cholesterol-catabolic (cytochrome P450) pathway in lesion-macrophages.

9. Angiotensin II enhances foam cell formation by upregulating ACAT1 expression predominantly through the actions of AT(1) receptor via the G protein/c-Src/PKC/MAPK pathway in human monocyte-macrophages

10. Docosahexaenoic acid can act as a substrate for ACAT1. In the manner of a poor substrate, docosahexaenoic acid also inhibited the activity of ACAT1.

11. Results suggest that the ERK, p38MAPK and JNK signaling pathways may be involved in insulin-mediated regulation of ACAT1, but no PI3K and PLC-gamma signaling pathways were involved in the present study.

12. Leptin accelerates cholesteryl ester accumulation in human monocyte-derived macrophages by increasing ACAT-1 expression.

13. High ACAT1 expression is associated with estrogen receptor negative basal-like breast cancer.

14. Macrophages cope with cholesterol loading by using a novel mechanism: they produce more ER-derived vesicles with elevated ACAT1 enzyme activity without having to produce more ACAT1 protein.

15. the plaque-modulating effects of K-604 can be explained by stimulation of procollagen production independent of ACAT inhibition in addition to potent inhibition of macrophage ACAT-1

16. Visfatin may down-regulate the ABCA1 expression and up-regulate the ACAT1 expression via PPARgamma signal transduction pathway, which decreases the outflow of free cholesterol, increases the content of cholesterol esters, and then induces foam cell formation.

17. In THP-1-derived macrophages and foam cells, the expression level of ACAT-1 and cellular cholesterol content increased significantly in response to asymmetric dimethylarginine treatment in a time- and concentration-dependent manner.

18. The present study shows that the C allele carriers of ACAT-1 rs1044925 SNP in male hyperlipidemic subjects had higher serum total cholesterol, HDL-cholesterol and ApoAI levels than the C allele noncarriers.

19. Essential oil of Pinus koraiensis leaves significantly inhibited hACAT1 levels in HepG2 cells.

20. Several lipid-related gene polymorphisms interact with overweight/obesity to modulate blood pressure levels.

Mouse (Murine) Sterol O-Acyltransferase 1 (SOAT1) interaction partners

1. NLRP3 is involved in the aggravation of cutaneous xanthomatosis and atherosclerosis in mice with bone marrow ACAT1 deficiency.

2. loss of ACAT1 in bone marrow-derived cells attenuates atherosclerosis, which is aggravated by the loss of NCEH1

3. blocking Soat1 (ACAT-1) suppresses diet-induced obesity in part by slowing down monocyte infiltration to white adipose tissue as well as by reducing the inflammatory responses of adipose tissue macrophage

4. results demonstrate that ACATs are required for storage ability of lipids and cholesterol in adipocytes

5. Soat-1 role in atherosclerosis

6. SOAT1 plays an important role in hypothalamic insulin sensitivity, linked to cognitive impairment, in high fat diet-fed mice.

7. a potential regulatory relationship between the sterol O-acetyltransferase 1 gene and Hoxc13 gene

8. A potentially novel gene or known gene with a novel phenotype resides within this interval, which may shed light on human diseases with defects in the inner structure of the hair fibre.

9. Soat1 is a quantitative trait loci gene contributing to hyperlipidemia.

10. soat1 had an important role in normal hair formation

11. ACAT1 activity plays a central role in the proper trafficking of cholesterol and in cholesterol-sensing in the macrophage.