ACAT1 Antibody, mAb, Mouse
- Known as:
- ACAT1 Antibody, mAb, Mouse
- Catalog number:
- A00082
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- ACAT1 Antibody mAb Mouse
Ask about this productRelated genes to: ACAT1 Antibody, mAb, Mouse
- 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 Antibody, mAb, Mouse
Related articles to: ACAT1 Antibody, mAb, Mouse
- The kappa class of glutathione S-transferases 1 (GSTK1) is a vital regulatory factor in metabolic diseases. This study was conducted to investigate the regulatory effects of GSTK1 on renal ectopic fat deposition (EFD) and lipotoxic injury in diabetic nephropathy (DN) . - Source: PubMed
Publication date: 2026/04/30
Chen HongLiu YanZhao Ming-GeWu Xue-QinDai Ai-MingWang YuYang Ye-YiLi Ai-MeiZhang WeiWang Jun-PuZhou Zhi-JiaoTi-Chen Zhang HaoYang Shikun - - Source: PubMed
Publication date: 2026/04/16
Wang LChen X HZhao P WFeng L F - Ulcerative colitis (UC), a chronic inflammatory bowel disorder characterized by progressive colonic inflammation, presents escalating global incidence rates and heightened risk of colorectal carcinogenesis. Despite emerging evidence implicating lactylation - a novel post-translational modification - in diverse biological pathways, its mechanistic involvement in UC pathogenesis remains poorly elucidated. Through integrative analysis of GEO datasets, we systematically identified lactylation-associated signatures in UC using differential expression profiling, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction network reconstruction. Six machine learning algorithms (Gaussian Mixture Model, Support Vector Machine, Random Forest, Gradient Boosting Machine, XGBoost, and LASSO regression) converged to identify ACAT1 as the central lactylation-associated hub gene. Comprehensive immune microenvironment profiling incorporating CIBERSORT deconvolution, single-sample gene set enrichment analysis (ssGSEA), and single-cell RNA sequencing (SEURAT/CellChat) revealed significant myeloid cell heterogeneity between healthy and UC cohorts, with Mendelian randomization analysis confirming causal immune-UC relationships. Clinical correlation analysis demonstrated marked ACAT1 downregulation in active UC phases, showing positive associations with M2 macrophage infiltration and resting mast cells, but inverse correlations with neutrophil activation and dendritic cell maturation. Building on the above signature, we mined the cMAP repository and retrieved sulfasalazine as an ACAT1-directed small molecule; molecular docking was subsequently employed to assess the predicted binding pose and affinity. Mechanistically, ACAT1 overexpression in colonic epithelial cells attenuated lactate accumulation and suppressed lactylation modifications in both in vitro and dextran sulfate sodium-induced murine colitis models. Our findings establish ACAT1 as a master regulator of lactate metabolism and protein lactylation in UC pathogenesis. The developed lactylation subtype stratification system and elucidated immune-stromal interaction network provide novel mechanistic insights, positioning ACAT1 as a potential diagnostic biomarker and therapeutic target for precision UC management. - Source: PubMed
Publication date: 2026/04/08
Yan JiayuLin ShanshanChen ZhuosiZhou ShuqingZhao YuluWang WeiweiWang ZifanFeng YubinLuo Lianxiang - Nonalcoholic fatty liver disease (NAFLD) is a major clinical challenge and a growing global public health burden, yet no pharmacological therapy specific to this disease has been approved to date. Notably, Astragalus membranaceus (Huangqi, HQ) is incorporated into approximately 80% of multi-herb formulations employed for treating liver diseases. Fuzhuan brick tea, a distinctive Chinese fermented tea, is widely recognized for its unique fermentation process and hypolipidemic properties. However, whether co-fermentation with HQ enhances its lipid-lowering efficacy against NAFLD remains unexplored and unreported. - Source: PubMed
Publication date: 2026/03/31
Chen TingYang ShusenZhang XinyueChen JuanYang XinkeLi ChengjunYang MingjieLi JingtaoJi XumingYan Shuguang - Polyubiquitination is a process whereby multiple ubiquitin proteins link to each other on a target substrate, marking that substate for various cellular processes of which protein degradation via the proteasome is the most common. Recently, evidence has emerged suggesting that the most common forms of proteasome-dependent (K48) and proteasome-independent (K63, M1) polyubiquitination have sex-specific roles in contextual fear memory formation in the amygdala and hippocampus. However, there are 8 different linkage sites at which polyubiquitin chains can form, most of which have not been studied in the brain. Lysine 27 (K27) polyubiquitination is a less common, non-canonical mark that has not been well studied and may be connected to the protein degradation process. To date, K27 polyubiquitination has never been examined in the brain under any condition. Here, we found that K27 polyubiquitination was selectively increased in the hippocampus after contextual fear conditioning in female, but not male, rats, though neither sex showed changes in this polyubiquitin mark in the amygdala. Consistent with this, CRISPR-dCas13-mediated knockdown of K27 polyubiquitination in the hippocampus selectively impaired contextual fear memory retention in the hippocampus of females, but not males. Proteomic analyses revealed ACAT1 as a target of K27 polyubiquitination in the female hippocampus following fear conditioning, though this mark was not associated with degradation of the target protein. Together, these data suggest that K27 polyubiquitination has a sex-selective role in fear memory formation in the hippocampus. These findings advance our understanding of molecular mechanisms of fear memory formation and the importance of sex as a biological variable in this process. - Source: PubMed
Publication date: 2026/03/27
Patrick Morgan BKincaid Shannon EArndt Kaiser CBae YeeunBall Olivia NCummings AdamAbraham Jennifer RBhanot GitaliRay W KeithJarome Timothy J