Ask about this productRelated genes to: ACOT12 antibody
- 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 antibody
Related articles to: ACOT12 antibody
- 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 - Dysregulation of mevalonate pathway, an essential metabolic route involving coenzyme A (CoASH) and cholesterol, contributes significantly to escalating cartilage degradation. Existing treatments rely on the simvastatin delivery tunable sol-gel transition mechanisms of injectable hydrogel. However, those methods suffer from lack of controllable drug release by selective phase transition under distinct disease microenvironment. Herein, we developed an aberrant lipid metabolism microenvironment-activated phase transition (normal condition: gel-gel, abnormal condition: gel-sol) with targeted drug release for synergistic treatment of osteoarthritis (OA). Naked-eye diagnosis and therapy of OA through cholesterol downregulation using an injectable hydrogel were based on the simvastatin-loaded nanoparticles embedded in hexanoyl glycol chitosan (HGC-SIM@PAA-MnO-cPDA or SIM gel). The interaction between highly expressed CoASH in OA and PAA-MnO in SIM gel altered the hydrophobic-hydrophilic balance and gelation temperature, triggering the OA-sensitive gel-sol transformation. Naked-eye gel-sol transformation was observed after incubating SIM gel with OA chondrocyte models, including acetyl-CoA-induced wild-type (WT + CoA), knockout (N7KO), and knockout (A12KO). Because of the simvastatin release after gel-sol transition, OA-related enzymes and genes, including antioxidant enzymes (), cartilage degradation genes (), and cholesterol synthesis-related enzymes (), were downregulated. studies revealed gel-sol transformation in destabilized medial meniscus of OA mice (DMM WT, N7KO, and A12KO) at 4-8 weeks post-injection, with significantly reduced cartilage degradation, demonstrating theragnostic capability of SIM gel. Thus, SIM gel offers a potential approach for future synergistic OA diagnosis and therapy. - Source: PubMed
Publication date: 2025/06/28
Robby Akhmad IrhasKim Ee HyunHuh Kang MooJin Eun-JungPark Ki DongPark Sung Young