Acetyl-CoA Acetyltransferase 1 (ACAT1) ELISA Kits

Human Acetyl-CoA Acetyltransferase 1 (ACAT1) Interaktionspartner

1. Silencing ACAT1 attenuates Abeta-induced cytotoxicity and cell apoptosis in SH-SY5Y cells, which may due to the synergistic effect of ACAT1 and COX2 through PKC/ERK pathways.

2. High ACAT1 expression is associated with breast cancer.

3. Insulin promotes progression of colon cancer by upregulation of ACAT1.

4. ACAT1 exonic mutations that affect ESE sequences may result in aberrant splicing. This may affect the activity of mitochondrial acetoacetyl-CoA thiolase.

5. compound heterozygous of ACAT1 gene mutations probably underlie the beta-ketothiolase deficiency in our patient

6. Data indicate that acetyl-CoA acetyltransferase (ACAT1) and malate dehydrogenase (MDH2) are involved in various drug-resistance-forming mechanisms.

7. ACAT1, ACACA, ALDH6A1 and MTHFD1 represent novel biomarkers in adipose tissue associated with type 2 diabetes in obese individuals.

8. the pyruvate dehydrogenase complex is regulated by Tyr phosphorylation of PDP1, which toggles recruitment between ACAT1 and SIRT3

9. these findings indicate that ACAT1 expression could serve as a potential prognostic marker in prostate cancer, specifically in differentiating indolent and aggressive forms of cancer.

10. ACAT1 expression is substantially elevated in human castration-resistant metastatic prostate cancer tissues.

11. Data show that the ketone body metabolizing enzymes BDH1, BDH2, OXCT1 and ACAT1 were expressed at the mRNA and protein level in all glioma cell lines.

12. We herein identified a common mutation, R208X, in Vietnamese patients. We identified R208X homozygously in six patients and heterozygously in two patients among eight Vietnamese patients.

13. the siblings with the same T2 gene mutations present different clinical severity of T2 deficiency

14. Single base substitutions at the initiator codon produced wild-type T2 polypeptide to various degrees

15. "mild" mutations (A132G, D339-V340insD) retained some residual T2 activity

16. Cloning and sequencing long range PCR products revealed a 6.4kb deletion. Alu element-mediated unequal homologous recombination between an Alu-Sx in intron 1 and another Alu-Y in intron 4 appears to be responsible for this deletion.

17. E252del is a temperature-sensitive K(m) mutant.

18. Crystallographic and kinetic studies were made on mitochondrial acetyl-CoA thiolase: the importance of potassium and chloride ions were noted for its structure and function.

19. A point mutation was responsible for the aberrant RNA splicing of the mitochondrial acetoacetyl-CoA thiolase gene.

20. sequence recognition by the catalytic domain differs between hT2 and hT10 in that hT10 requires a pre-existing GalNAc residue while hT2 does not

Mouse (Murine) Acetyl-CoA Acetyltransferase 1 (ACAT1) Interaktionspartner

1. A Soat1 deletion present in AKR mice, and resultant N-terminal ACAT1 truncation, was confirmed to be a significant modifier of macrophage cholesterol metabolism.

2. Data show that microRNA miR-467b regulates the acetyl-CoA acetyltransferase 1 (ACAT1) expression via targeting ACAT1 3' untranslated regions (3'UTR).

3. In a mouse model, targeting ACAT1 specifically in a myeloid lineage may benefit atherosclerosis progression by reducing the infiltration of foamy macrophages.

4. Its blockage enhances autophagy of and reduces human p301L-tau content in brain neurons of pre-symptomatic stage of Alzheimer disease.

5. Oxidized low-density lipoprotein activated the TLR4/MyD88/NF-kappaB inflammatory signaling pathway in vascular smooth muscle cell, which upregulates the ACAT1 expression and promotes VSMC foam cell formation.

6. Exacerbation of liver fibrosis by ACAT1 deficiency was dependent on free cholesterol accumulation-induced enhancement of TLR4 signaling.

7. ACAT1 plays important roles in hematopoiesis in normal mouse and in Apoe(-/-) mouse during atherosclerosis development.

8. ApoA-I Helsinki promotes accumulation of ACAT1 in a mouse macrophage cell line.

9. 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

10. ACAT1 gene ablation increases 24(S)-hydroxycholesterol content in the brain and ameliorates amyloid pathology in mice with Alzheimer disease.

11. ACAT1 displays less capacity than ACAT2 to differentiate cholesterol from sitosterol

12. ACAT1 knockout macrophages show biochemical changes consistent with increased cytotoxicity and also a novel association with decreased expression of collagen type 3A1.

13. Deficiency of macrophage ACAT1 accelerates atherosclerosis in apoE-/- mice but has no effect when hypercholesterolemia is corrected by apoE expression. ACAT1 deletion impairs ABCA1-mediated cholesterol efflux in macrophages regardless of apoE expression

14. sitosterol-induced macrophage death does not require ACAT dysfunction and so may occur in an accelerated fashion

15. Report differential effects of PARP-1 inhibition on vascular cell survival and ACAT-1 expression favouring atherosclerotic plaque stability.

Cow (Bovine) Acetyl-CoA Acetyltransferase 1 (ACAT1) Interaktionspartner

1. The transcript abundance of ACAT1 was increased in the more efficient low residual feed intake (RFI) animals and decreased in the less efficient high RFI animals