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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 Proteins (13) 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 ELISA Kits) and SREBP-1 (show SREBF1 ELISA Kits) on tumor growth.
Our results demonstrated the contrasting effects of STC1 (show STC1 ELISA Kits) and STC2 (show STC2 ELISA Kits)-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 ELISA Kits) expression, lower SOAT1 (show SOAT1 ELISA Kits) and higher SQLE (show SQLE ELISA Kits) expression. Besides high SQLE (show SQLE ELISA Kits) expression, cancers that became lethal despite primary treatment were characterized by low LDLR (show LDLR ELISA Kits) expression (odds ratio for highest versus lowest quintile, 0.37; 95% CI 0.18-0.76) and by low SOAT1 (show SOAT1 ELISA Kits) 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 ELISA Kits) siRNA inhibits cell proliferation, migration and invasion by suppressing ACAT1 expression, suggesting that TLR4 (show TLR4 ELISA Kits) 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 ELISA Kits)-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 (show AKT1 ELISA Kits) and/or the ERK1/2 (show MAPK1/3 ELISA Kits) pathway.
Data indicate that mitotane confers adrenal-specific cytotoxicity and down-regulates steroidogenesis by inhibition of sterol-O-acyl-transferase 1 (SOAT1 (show SOAT1 ELISA Kits)) leading to lipid-induced endoplasmic reticulum (ER) stress.
Data show that microRNA miR (show MLXIP ELISA Kits)-467b regulates the acetyl-CoA acetyltransferase 1 (ACAT1) expression via targeting ACAT1 (show SOAT1 ELISA Kits) 3' untranslated regions (3'UTR (show UTS2R ELISA Kits)).
In a mouse model, targeting ACAT1 (show SOAT1 ELISA Kits) 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 ELISA Kits)/MyD88 (show MYD88 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) inflammatory signaling pathway in vascular smooth muscle cell, which upregulates the ACAT1 (show SOAT1 ELISA Kits) expression and promotes VSMC foam cell formation.
Exacerbation of liver fibrosis by ACAT1 (show SOAT1 ELISA Kits) deficiency was dependent on free cholesterol accumulation-induced enhancement of TLR4 (show TLR4 ELISA Kits) signaling.
ACAT1 (show SOAT1 ELISA Kits) plays important roles in hematopoiesis in normal mouse and in Apoe (show APOE ELISA Kits)(-/-) mouse during atherosclerosis development.
ApoA-I (show APOA1 ELISA Kits) Helsinki promotes accumulation of ACAT1 (show SOAT1 ELISA Kits) 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 ELISA Kits) inhibition in addition to potent inhibition of macrophage ACAT-1 (show SOAT1 ELISA Kits)
ACAT1 (show SOAT1 ELISA Kits) 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 ELISA Kits) 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) animals and decreased in the less efficient high RFI 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