ACAT1
- Known as:
- ACAT1
- Catalog number:
- 000987A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACAT1
Related genes to: ACAT1
- Gene:
- ACAT1 NIH gene
- Name:
- acetyl-CoA acetyltransferase 1
- Previous symbol:
- ACAT
- Synonyms:
- THIL
- Chromosome:
- 11q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-12
- Date modifiied:
- 2014-11-19
Related products to: ACAT1
ACACT,ACACT1,ACAT,ACAT1,ACAT-1,Acyl-coenzyme A cholesterol acyltransferase 1,Cholesterol acyltransferase 1,Homo sapiens,Human,SOAT,SOAT1,STAT,Sterol O-acyltransferase 1ACAP2 Gene ArfGAP with coiled-coil, ankyrin repeat and PH domains 2ACAT,ACAT1,Acetoacetyl-CoA thiolase,Acetyl-CoA acetyltransferase, mitochondrial,Homo sapiens,Human,MAT,T2acat1 antibody Isotype IgG Host RabbitACAT1 MAT antibody Ab host: RabbitACAT1 MAT antibody Ab host: RabbitACAT1 MAT (253-266) antibody Ab host: GoatACAT1 MAT (257-269) antibody Ab host: GoatACAT1 MAT (C-term) Ig antibody Ab host: RabbitACAT1 MAT (N-term) IgG antibody Ab host: MouseACAT1 MAT IgG antibody Ab host: RabbitACAT1 MAT IgG antibody Ab host: RabbitACAT1 MAT IgG antibody Ab host: RabbitACAT1 MAT IgG1 antibody Ab host: MouseACAT1 MAT IgG1 antibody Ab host: Mouse Related articles to: ACAT1
- Beta-ketothiolase deficiency (BKTD) is a rare autosomal recessive metabolic disorder affecting isoleucine catabolism and ketone body utilization, demonstrating marked clinical and biochemical heterogeneity. This study aims to characterize the longitudinal clinical, biochemical, and genetic features of a single-center BKTD cohort and evaluate phase-dependent dynamics in metabolic biomarkers during acute crises and stable follow-up periods. - Source: PubMed
Publication date: 2026/08/25
Ergun Nurcan ÜçüncüCoşkun NihalAslantaş MerveKöse Meyrem Aybike Kurtbeyoğlu - Beta-ketothiolase deficiency (BKTD) is a rare genetic metabolic disorder caused by variants in the ACAT1 gene. It can induce severe metabolic acidosis, which may be life-threatening. This study reports two critically ill children with newly diagnosed BKTD and includes a literature review to comprehensively depict the clinical, biochemical, and genetic profiles of BKTD patients in China. - Source: PubMed
Publication date: 2026/08/19
Deng XiLi XintingLiu HaoranWang TaoTang FangTan QingtiFeng YuLuo Xiaoli - Major depressive disorder (MDD) and obesity are intersecting global crises. Despite observational links, a clinical paradox persists: antidepressants often improve metabolic status, while weight loss rarely alleviates core depressive symptoms. This prompts closer examination of whether the depression-obesity relationship reflects asymmetric genetic architecture, shared liability, or statistical constraints that obscure definitive conclusions. - Source: PubMed
Publication date: 2026/08/07
Li XingpeiChen ChunlinLi HuibingHe YiruTang KailangLai GuanqiaoYang ZiyangChen WushuYang Huihui - Protein post-translational modification (PTM) plays a significant role in the progression of atherosclerosis (AS). However, the role of O-GlcNAcylation, as an important O-glycosylation modification, in the formation of foam cells remains unclear, limiting early diagnosis and mechanistic studies. Here, utilizing two bioorthogonal reactions, we developed a ratiometric fluorescent nanoprobe-based tracker for O-GlcNAcylation. This tracker (BORFI) enables dynamic tracing, relative quantification, and multi-scale in situ visualization of protein O-GlcNAcylation during cellular events, and images the regulation of O-GlcNAcylation during foam cell formation. Using BORFI, we successfully achieved spatiotemporal co-imaging of O-GlcNAcylation and reactive oxygen species (ROS), and found that there is a significant positive correlation between O-GlcNAcylation and ROS during the transition from macrophages to foam cells. Treatment with the OGT enzyme inhibitor (OSMI-1) to affect the O-GlcNAcylation level in foam cells effectively alleviates foam cell formation, accompanied by suppression of the overall increase in ROS levels, modulation of key cholesterol metabolism‑related proteins (downregulation of ACAT1 and upregulation of ABCA1), and downregulation of the scavenger receptor MSR1. Furthermore, BORFI was successfully applied to in situ imaging of the aorta in a mouse AS model, and we found that hyperglycemia participates in AS progression by specifically upregulating vascular O-GlcNAcylation. - Source: PubMed
Publication date: 2026/08/13
Xu JihengZhang WeiLi PingTang YueZhang WenWang HuiTang Bo - Ionizing radiation (IR)-induced alterations in glucose metabolism are closely associated with radioresistance, yet the underlying mechanisms remain incompletely understood. Here, we identify a post-translational modification axis in which IR induces general control non-repressible protein 5 (GCN5/KAT2A)-mediated crotonylation of acetyl-CoA acetyltransferase 1 (ACAT1) at lysine 181 (K181), thereby enhancing ACAT1 activity and promoting increased acetylation of pyruvate dehydrogenase E1 subunit alpha (PDHA1) along with its phosphorylation at S293.These changes led to inhibition of PDHA1, impaired pyruvate metabolism, and increased lactate accumulation. Functional studies demonstrated that ACAT1 K181R (a decrotonylation-mimicking mutant) increased radiosensitivity and significantly attenuated IR-induced lactate production. Collectively, these findings reveal an unrecognized mechanism by which radiotherapy reprograms cellular metabolism through the GCN5-ACAT1-PDHA1 axis, linking ACAT1 crotonylation to altered pyruvate metabolism, enhanced lactate production, and subsequent radioresistance. These findings suggest that targeting ACAT1 K181 crotonylation represents a potential therapeutic strategy to improve tumor radiosensitivity. - Source: PubMed
Publication date: 2026/07/23
Chen ShiLi SaiyuGuo HejiangGao ShuainingGao YueDing LehanZhao BinZhong KunGuan HuaPeng Rui-YunZhou Ping-Kun