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ACAT1 encodes a mitochondrially localized enzyme that catalyzes the reversible formation of acetoacetyl-CoA from two molecules of acetyl-CoA. Additionally we are shipping ACAT1 Antibodies (164) and ACAT1 Kits (18) and many more products for this protein.
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Intracranial GBM xenografts were used to determine the effects of genetically silencing SOAT1 (show SOAT1 Proteins) and SREBP-1 (show SREBF1 Proteins) on tumor growth.
Our results demonstrated the contrasting effects of STC1 (show STC1 Proteins) and STC2 (show STC2 Proteins)-derived peptides on human macrophage foam cell formation associated with ACAT1 expression and on HASMC migration.
Higher Gleason grade was associated with lower LDLR (show LDLR Proteins) expression, lower SOAT1 (show SOAT1 Proteins) and higher SQLE (show SQLE Proteins) expression. Besides high SQLE (show SQLE Proteins) expression, cancers that became lethal despite primary treatment were characterized by low LDLR (show LDLR Proteins) expression (odds ratio for highest versus lowest quintile, 0.37; 95% CI 0.18-0.76) and by low SOAT1 (show SOAT1 Proteins) expression (odds ratio, 0.41; 95% CI 0.21-0.83).
these results illustrate that ACAT1-catalyzed esterification of 24S-OHC with long-chain unsaturated fatty acid followed by formation of atypical LD-like structures at the ER membrane is a critical requirement for 24S-OHC-induced cell death.
ACAT1 exonic mutations that affect ESE sequences may result in aberrant splicing. This may affect the activity of mitochondrial acetoacetyl-CoA thiolase.
TLR4 (show TLR4 Proteins) siRNA inhibits cell proliferation, migration and invasion by suppressing ACAT1 expression, suggesting that TLR4 (show TLR4 Proteins) may be a potential therapeutic target for the treatment of colorectal cancer
ACAT1 has a role in regulating the dynamics of free cholesterols in plasma membrane which leads to the APP (show APP Proteins)-alpha-processing alteration
compound heterozygous of ACAT1 gene mutations probably underlie the beta-ketothiolase deficiency in our patient
ACAT1 regulates glioblastoma-cell proliferation via modification of the Akt and/or the ERK1/2 pathway.
Data indicate that mitotane confers adrenal-specific cytotoxicity and down-regulates steroidogenesis by inhibition of sterol-O-acyl-transferase 1 (SOAT1 (show SOAT1 Proteins)) leading to lipid-induced endoplasmic reticulum (ER) stress.
Data show that microRNA miR (show MLXIP Proteins)-467b regulates the acetyl-CoA acetyltransferase 1 (ACAT1) expression via targeting ACAT1 (show SOAT1 Proteins) 3' untranslated regions (3'UTR).
In a mouse model, targeting ACAT1 (show SOAT1 Proteins) specifically in a myeloid lineage may benefit atherosclerosis progression by reducing the infiltration of foamy macrophages.
Oxidized low-density lipoprotein activated the TLR4 (show TLR4 Proteins)/MyD88 (show MYD88 Proteins)/NF-kappaB (show NFKB1 Proteins) inflammatory signaling pathway in vascular smooth muscle cell, which upregulates the ACAT1 (show SOAT1 Proteins) expression and promotes VSMC foam cell formation.
Exacerbation of liver fibrosis by ACAT1 (show SOAT1 Proteins) deficiency was dependent on free cholesterol accumulation-induced enhancement of TLR4 (show TLR4 Proteins) signaling.
ACAT1 (show SOAT1 Proteins) plays important roles in hematopoiesis in normal mouse and in Apoe (show APOE Proteins)(-/-) mouse during atherosclerosis development.
ApoA-I (show APOA1 Proteins) Helsinki promotes accumulation of ACAT1 (show SOAT1 Proteins) in a mouse macrophage cell line.
the plaque-modulating effects of K-604 can be explained by stimulation of procollagen production independent of ACAT (show SOAT1 Proteins) inhibition in addition to potent inhibition of macrophage ACAT-1 (show SOAT1 Proteins)
ACAT1 (show SOAT1 Proteins) gene ablation increases 24(S)-hydroxycholesterol content in the brain and ameliorates amyloid pathology in mice with Alzheimer disease.
ACAT1 displays less capacity than ACAT2 to differentiate cholesterol from sitosterol
ACAT1 (show SOAT1 Proteins) knockout macrophages show biochemical changes consistent with increased cytotoxicity and also a novel association with decreased expression of collagen type 3A1.
The transcript abundance of ACAT1 was increased in the more efficient low residual feed intake (RFI (show RNF34 Proteins)) animals and decreased in the less efficient high RFI (show RNF34 Proteins) animals
The protein encoded by this gene belongs to the acyltransferase family. It is located in the endoplasmic reticulum, and catalyzes the formation of fatty acid-cholesterol esters. This gene has been implicated in the formation of beta-amyloid and atherosclerotic plaques by controlling the equilibrium between free cholesterol and cytoplasmic cholesteryl esters. Alternatively spliced transcript variants have been found for this gene.
acetoacetyl Coenzyme A thiolase
, acetoacetyl-CoA thiolase
, acetyl-CoA acetyltransferase, mitochondrial
, acetyl-Coenzyme A acetyltransferase 1
, mitochondrial acetoacetyl-CoA thiolase
, acyl-coenzyme A:cholesterol acyltransferase 1
, sterol O-acyltransferase (acyl-Coenzyme A: cholesterol acyltransferase) 1
, acetyl-Co A acetyltransferase 1 mitochondrial
, acetyl-coenzyme A acetyltransferase 1
, acetyl-Coenzyme A acetyltransferase 1 (acetoacetyl Coenzyme A thiolase)
, acetyl-CoA acetyltransferase 1
, Acetoacetyl-CoA thiolase A
, acetyl-CoA acetyltransferase A, mitochondrial