ACOT12
- Known as:
- ACOT12
- Catalog number:
- 001024A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACOT12
Related genes to: ACOT12
- Gene:
- ACOT12 NIH gene
- Name:
- acyl-CoA thioesterase 12
- Previous symbol:
- -
- Synonyms:
- Cach, THEAL, STARD15
- Chromosome:
- 5q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-08
- Date modifiied:
- 2014-11-18
Related products to: ACOT12
Related articles to: ACOT12
- Intermittent fasting (IF) ameliorates metabolic dysfunction-associated steatotic liver disease (MASLD), but the underlying mechanism remains unclear. Combined CUT&Run and transcriptomic analysis shows that hepatic Ahcy is controlled by the super‑enhancer (SE) and acts as a key mediator of IF's benefit. Liver‑specific Ahcy knockout worsens high‑fat diet (HFD)‑induced hepatic steatosis and blunts the protective effect of IF. Furthermore, inhibition of Brd4 or deletion of the core SE region reduces Ahcy expression and exacerbates lipid accumulation in vivo or in vitro. Hnf4a is identified as the transcription factor driving the Ahcy-SE. In vitro and in vivo experiments demonstrate that IF-activated Hnf4a directly binds to and activates the Ahcy-SE. Ahcy knockdown attenuates the lipid-deposition-reducing effect of Hnf4a overexpression in mice fed a HFD. In Ahcy mice, the liver SAM/SAH ratio is reduced, and Reduced Representation Bisulfite Sequencing (RRBS) and transcriptome sequencing reveal liver-specific methylation remodeling. One manifestation of this remodeling is hypermethylation of metabolic gene promoters, including the Acot12 promoter, where aberrant recruitment of Dnmt3b leads to silencing of the gene and impaired lipid hydrolysis. Therefore, these findings define an IF-Hnf4a-Ahcy pathway that activates SE-driven Ahcy to orchestrate protective epigenetic reprogramming in MASLD. - Source: PubMed
Publication date: 2026/07/27
Chen HuafengZhang ShilinDeng XiaojieXie WenqiangXu FenShen JieLiang Hua - Cardiovascular diseases are a major global health burden, demanding phenotyping frameworks that can match the scale and complexity of contemporary mouse genetics. Here, we introduce EchoVisuALL, an AI-enabled pipeline for automated high-throughput transthoracic echocardiography (TTE) coupling deep-learning-based left-ventricular segmentation with data reporting. Across 65,000 recordings from over 18,000 mice, including single-gene knockouts from the International Mouse Phenotyping Consortium, the framework quantified cardiac morphology and function with minimal operator dependency and high reliability, validated against an expert-curated gold standard dataset. By extracting quantitative parameters across the cardiac cycle, EchoVisuALL in combination with multi-dimensional clustering uncovered nonlinear phenotypic relationships and revealed 37 of 715 genes associated with significant cardiac abnormalities, encompassing well-known human disease genes as well as 12 previously unrecognized candidates, including , , , , , and . These genotype-phenotype associations are involved in myocardial energetics, membrane biology, and cardiac remodeling. We demonstrate the potential of EchoVisuALL to move beyond image segmentation by delivering a standardized, quantitative foundation for scalable downstream analyses, enabling the discovery of novel cardiac disease genes. - Source: PubMed
Publication date: 2026/02/19
Galter IsabellaSchneltzer ElidaMarr CarstenSpielmann NadineHrabě de Angelis Martin - Sheep have diversified into distinct breeds worldwide through both natural adaptation and human-driven selection, with hybridization serving as an effective strategy for rapid trait improvement. The Tianhua mutton sheep (TMS) is a novel breed derived from crossing South African Mutton Merino (SAMM) with Gansu alpine fine-wool sheep (GAFS). After nearly two decades of selective breeding, TMS has developed great meat quality traits and impressive cold tolerance at high altitudes. To study the genetic mechanism and provide new insights into phenotypic variation, we analyzed the genetic diversity, population structure, and selective signatures of TMS based on whole-genome sequencing of 55 TMS, 11 SAMM, and 197 public sheep genomes worldwide. - Source: PubMed
Publication date: 2026/01/31
Jiang BeixiangZeng JizeChi HuanpengShan JingfangZhang XueyingFeng QianjieLi FadiYue XiangpengFu Weiwei - The SARS-CoV-2 nucleocapsid (N) protein plays a pivotal role in disrupting host cellular processes by interfering with G3BP1, a key stress granule protein involved in RNA binding and metabolic regulation. Using RNA immunoprecipitation coupled with nanopore sequencing, we found that the N protein significantly alters the RNA interactome of G3BP1, particularly reducing binding to transcripts involved in fatty acid metabolism, such as ACOT12, PLIN4, GPX1, and ACADS. This disruption leads to dysregulation of lipid homeostasis and stress granule assembly, suggesting a strategy of the virus to reprogram host metabolism for its advantage. We also found that the N protein of the Wuhan strain exhibits stronger G3BP1 binding than that of the Omicron variant, potentially contributing to differences in pathogenicity. Mendelian randomization identified dihomolinoleate (20:2n6), an omega-6 polyunsaturated fatty acid, as a protective factor against severe COVID-19, while 4-androsten-3beta,17beta-diol disulfate, a steroid hormone metabolite, was associated with increased disease severity. These findings highlight the critical role of lipid metabolism in COVID-19 pathogenesis. The upregulation of the dihomolinoleate metabolic pathway genes in COVID-19 patients further underscores the importance of metabolic reprogramming during infection. - Source: PubMed
Publication date: 2025/10/30
Yin YipingChen JunkaiChen SiweiHuang JuLiu FengqiLiu ZhixinTong Zhaohui - Ankylosing spondylitis (AS) displays wide inter-patient variability that is not accounted for by HLA-B27 alone, suggesting that additional immune and metabolic modifiers contribute to disease severity. Using a genetically matched design, we profiled peripheral blood mononuclear cells from two brother pairs discordant for AS severity and one healthy brother pair. Strand-specific RNA-seq was analyzed with a family-blocked DESeq2 model, while untargeted metabolites were quantified using gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-mass spectrometry (LC-MS). Differential features were defined as follows: differentially expressed genes (DEGs) (|logFC| ≥ 1 and FDR < 0.05) and metabolites (VIP > 1, FC ≥ 1.2, and BH-adjusted < 0.05). Pathway enrichment was performed with KEGG and Gene Ontology (GO). A total of 325 genes were differentially expressed. Type I interferon and neutrophil granule transcripts (e.g., , , ) were markedly up-regulated, whereas mitochondrial β-oxidation genes (, , ) were repressed. Metabolomics revealed 110 discriminant features, including 25 MS/MS-annotated metabolites. Primary bile acid intermediates were depleted, whereas oxidized fatty acid derivatives such as 12-Z-octadecadienal and palmitic amide accumulated. Spearman correlation identified two antagonistic modules (i) interferon/neutrophil genes linked to pro-oxidative lipids and (ii) lipid catabolism genes linked to bile acid species that persisted when severe and mild siblings were compared directly. Enrichment mapping associated these modules with viral defense, neutrophil degranulation, fatty acid β-oxidation, and bile acid biosynthesis pathways. This sibling-paired peripheral blood mononuclear cell (PBMC) dual-omics study delineates an interferon-driven lipid-bile acid axis that tracks AS severity, supporting composite PBMC-based biomarkers for future prospective validation and highlighting mitochondrial lipid clearance and bile acid homeostasis as potential therapeutic targets. - Source: PubMed
Publication date: 2025/08/16
Wang ZeHuang YiGuo ZiyuSun JianhuaZheng Guoquan