ACOT13
- Known as:
- ACOT13
- Catalog number:
- 001025A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACOT13
Ask about this productRelated genes to: ACOT13
- Gene:
- ACOT13 NIH gene
- Name:
- acyl-CoA thioesterase 13
- Previous symbol:
- THEM2
- Synonyms:
- HT012
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-02
- Date modifiied:
- 2016-10-05
Related products to: ACOT13
Related articles to: ACOT13
- This experiment was conducted to investigate the effects of mulberry leaf powder (MLP) on alleviating fatty liver hemorrhagic syndrome (FLHS) in laying hens. A total of 180 healthy 33-week-old Hy-Line Gray laying hens were randomly assigned to 3 groups, with 6 replicates per group and 10 chickens per replicate, and fed a basal diet (CON), high-energy-low-protein (HELP) diet (FLHS), and HELP + 5% MLP diet (MLP), respectively. The experiment lasted 56 days. Results showed that the HELP diet successfully induced FLHS, characterized by an increased liver index, hepatic steatosis, and oxidative stress (P < 0.05). MLP significantly alleviated FLHS-induced hepatic steatosis, and enhanced antioxidant capacity (superoxide dismutase, catalase, glutathione peroxidase, total antioxidant capacity, and glutathione) in serum and liver (P < 0.05). Transcriptomic analysis identified 102 differentially expressed genes, whose expression was increased by FLHS but reversed by MLP, including SREBF1, SLC27A4, PLIN2, ACOT13, APOA4, GLRX, and MSRB1, which mainly participate in lipid droplet dynamics and redox homeostasis. qRT-PCR confirmed that upregulated expression of lipogenic genes (such as FASN, ACACA, SCD, and ELOVL6) and the downregulated expression of oxidative stress-responsive genes (SOD1 and GPX1) in the FLHS group were normalized by MLP (P < 0.05), accompanied by increased expression of PPARα, CPT1A, and CD36 (P<0.05). 16S rRNA sequencing revealed that MLP reduced the abundance of Desulfovibrio, Rikenellaceae_RC9_gut_group, Intestinimonas, and Shuttleworthia, and enriched Faecalibacterium and Bifidobacterium in the cecum of FLHS laying hens (P < 0.05). Furthermore, MLP increased acetate, propionate, and butyrate levels, and decreased isobutyrate and isovalerate levels (P < 0.05). Correlation analysis showed that cecal acetate, propionate, butyrate, Faecalibacterium and Bifidobacterium were positively correlated with hepatic antioxidant enzyme activities (P < 0.05), and negatively correlated with hepatic lipogenic gene expression, hepatic lipid deposition and oxidative stress markers (P < 0.05). These findings indicated that MLP alleviated hepatic lipid metabolism disorders and oxidative stress in FLHS laying hens, which might be achieved by modulating gut microbiota structure and short-chain fatty acid production. - Source: PubMed
Publication date: 2026/07/16
Xuan LingLiu HongliZhang HengGao QingtaoShang YanLiu XuelanYan PeipeiShi TianhongFu Chunyan - Low back pain (LBP) is a widespread global health concern that profoundly impairs patients' quality of life and productivity. Intervertebral disc degeneration (IVDD) is considered a major pathological factor in low back pain, yet the underlying mechanisms of IVDD remain incompletely understood. Current treatment strategies primarily focus on symptomatic relief through medication or surgical removal of degenerated tissue, lacking effective interventions that can reverse the degenerative process. This study investigates the role of fatty acid metabolism in IVDD and proposes a novel therapeutic strategy. Through single-cell sequencing and multi-omics analysis of clinical samples, we identified ACOT13 as a key regulator of fatty acid metabolism. We demonstrated that under pathological conditions, ACOT13 inhibits the AMPK/ACC signaling pathway, leading to disrupted fatty acid metabolism, mitochondrial dysfunction, and subsequently, pyroptosis, which accelerates IVDD progression. Furthermore, we developed an innovative self-assembled nanoparticles based on a traditional Chinese medicine formula. Employing molecular dynamics simulations, we elucidate the self-assembly mechanism, identifying the core constituents and establishing the key roles of hydrophobic interactions, π-π stacking, and hydrogen bonding as the driving forces. Moreover, we revealed that this nano-formulation suppresses ACOT13 function, activates the AMPK/ACC pathway, and improves fatty acid metabolism and mitochondrial function, thereby suppressing pyroptosis and ultimately alleviating IVDD progression. In summary, this study explores a novel mechanism of IVDD from the perspective of fatty acid metabolism and identifies key active components (N-QJZG) from a traditional Chinese medicine decoction, providing new insights for IVDD treatment and promoting the modernization of traditional Chinese medicine research. - Source: PubMed
Publication date: 2026/02/08
Qi WeihuiYuan MingchaoHe DuDou FeiZhang DuodanLv KeYang JianyeMiao ZhiminZhang LiangpingMao XinningMei ZhenglinJin HongtingPan HaoWang Dong - Mitochondrial dysregulation contributes to the chemoresistance of multiple cancer types. Yet, the functions of mitochondrial dysregulation in Ovarian serous cystadenocarcinoma (OSC) remain largely unknown. - Source: PubMed
Publication date: 2024/12/29
Shen DongshengWu ChenghaoChen MeiyiZhou ZixuanLi HuaifangTong XiaowenChen ZhenghuGuo Yi - A novel valuable prognostic model has been developed on the basis of immune-related genes (IRGs), which could be used to estimate overall survival (OS) in ovarian cancer (OC) patients in The Cancer Genome Atlas (TCGA) dataset and the International Cancer Genome Consortium (ICGC) dataset. - Source: PubMed
Publication date: 2024/10/31
Yu MinLi DanZhang LiWang Ke - Coronary microembolization (CME) can result in cardiac dysfunction, severe arrhythmias, and a reduced coronary flow reserve. Impairment of mitochondrial energy metabolism has been implicated in the progression and pathogenesis of CME; however, its role remains largely undetermined. This study aimed to explore alterations in mitochondria-related genes in CME. - Source: PubMed
Publication date: 2024/09/23
Jiang ZhaochangLu HaohaoGao BeibeiHuang JinyuDing Yu