AADACL1
- Known as:
- AADACL1
- Catalog number:
- 000865A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AADACL1
Related genes to: AADACL1
- Gene:
- NCEH1 NIH gene
- Name:
- neutral cholesterol ester hydrolase 1
- Previous symbol:
- AADACL1
- Synonyms:
- KIAA1363, NCEH
- Chromosome:
- 3q26.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-25
- Date modifiied:
- 2014-11-19
Related products to: AADACL1
Related articles to: AADACL1
- Graves' disease (GD) is characterized by hyperthyroidism and is influenced by genetic and environmental factors. The "gut-thyroid axis" establishes a connection between the gut microbiota and GD, yet the underlying potential mechanisms remain unclear. This study employed Mendelian randomization to investigate the causal relationships between the gut microbiota and GD, aiming to identify key microbial taxa and their metabolites, as well as to explore the regulatory roles of relevant genes in the pathogenesis of GD. - Source: PubMed
Publication date: 2026/08/03
Zhang YuyingLi Jin'eLuo YunfeiLiu ShuangLiu Jianping - High-grade serous ovarian cancer (HGSC) is the most aggressive subtype of ovarian epithelial cancer (OEC), with characters of late-stage diagnosis, high recurrence rate, and poor survival outcomes. Fucosyltransferase 8 (FUT8) is responsible for α1,6-core fucosylation biosynthesis, and aberrant FUT8/α1,6-core fucosylation level is involved in tumor progression. However, the roles and mechanisms of protein FUT8 and α1,6-core fucosylation in HGSC tumorigenesis and progression remain elusive. Here, our study confirms that elevated levels of FUT8/α1,6-core fucose in the tissues and serum of HGSC patients, and the elevation is associated with poor patient prognosis. By applying glycoproteomic assay, we globally screen and identify NCEH1 as the specific scaffold protein of α1,6-core fucosylation. Alpha 1,6-core fucose modification stabilizes NCEH1 by preventing its degradation through proteasomal pathway. Importantly, combined with non-targeted metabolomics analysis, α1,6-core fucosylated NCEH1 facilitates LPA secretion, driving M2-like polarization of tumor-associated macrophages in the tumor microenvironment, thus leading to oncogenesis and peritoneal metastasis of HGSC in vitro and in vivo. These findings broaden the understanding of FUT8/α1,6-core fucosylation/NCEH1 in HGSC progression and metastasis, and offer glycosylated diagnostic indicators and targets for therapeutic strategies in HGSC. - Source: PubMed
Publication date: 2026/03/05
Pei XiaoSongWang FeiLiu XiaominLei YuyuChen YuLiu BoSun RuixuanLi PeiyuBi JianleiLiu Shuai - Neutral cholesterol ester hydrolase 1 (NCEH1), a key enzyme in cellular lipid metabolism, is associated with cancer progression. Its molecular functions in breast cancer remain poorly understood. - Source: PubMed
Publication date: 2026/01/27
Sun JieLiu YaqianMo JiejiZhou JialinBai XueGu BoshiLi JunZhao Haidong - Cadmium (Cd) exposure is an emerging environmental risk factor for atherosclerotic cardiovascular diseases (ASCVDs), particularly ischemic stroke (IS). MicroRNAs are potential mediators linking environmental exposure to health hazards. However, the role of miRNAs in the development of IS triggered by Cd exposure remains largely unknown. In this study, we first demonstrate that Cd exposure, even at a relatively low dosage (4 mg/L), significantly facilitates the progression of atherosclerosis in apolipoprotein E-deficient mice fed a high-fat diet. This pro-atherogenic effect was accompanied by comprehensive disturbances in systemic and vascular cholesterol homeostasis, evidenced by altered plasma lipid profiles, hepatic lipid accumulation, and dysregulated expression of key genes governing cholesterol uptake (), efflux (), and hydrolysis () within the aortic wall. Integrated transcriptomic and metabolomic analyses further corroborated the profound disruption of the lipid metabolism pathways. Through miRNA microarray, bioinformatics analysis, and qRT-PCR validation, we identified miR-30d-5p and miR-504-3p as novel epigenetic regulators mediating Cd-induced foam cell formation. Specifically, Cd treatment upregulated miR-30d-5p and downregulated miR-504-3p, which directly targeted and , respectively, thereby promoting intracellular lipid accumulation. In a case-control population (494 IS patients and 494 controls), plasma miR-30d-5p levels were positively associated with Cd exposure and partially mediated the Cd-stroke association, accounting for 16.4% of the total effect. Moreover, miR-30d-5p significantly improved the discrimination and reclassification of IS patients beyond the traditional risk factors. In summary, our findings reveal that Cd induces atherosclerosis by disrupting cholesterol homeostasis and modulating miRNA-regulated pathways with plasma miR-30d-5p serving as a potential biomarker and mediator for Cd-related ischemic stroke. Further perspective investigations are warranted to validate our findings. - Source: PubMed
Publication date: 2025/11/26
Wang TianLv ZiquanFu XuejunZhang YanweiZou DongjuChen JiaxinZou ZiyangLiu JinlingWang ChaoXiong YihanLin GuimiaoLiu YueweiLiu PeiyiCheng JinquanHuang Suli - This study aimed to identify phenotypic biomarkers associated with high-altitude adaptation in Bayinbuluke sheep and to investigate the correlations between serum biochemical parameters and muscle transcriptomic, metabolomic, and proteomic profiles. Bayinbuluke sheep (raised at 3200 m) and Turpan black sheep (raised at-154 m) were selected for the experiment. The results demonstrated that, to adapt to the complex high-altitude hypoxic environment, Bayinbuluke sheep enhance glycolytic flux to rapidly generate energy, suppress intramuscular lipid synthesis, regulate lipid metabolic homeostasis to maintain energy balance, and remodel metabolic networks. Specifically, the GPAT3 gene promotes neutral cholesterol ester hydrolase 1 (NCEH1) through the glycerophospholipid metabolism pathway, facilitating the hydrolysis of cholesterol esters and fatty acid esters, thereby modulating systemic lipid metabolism. The FASN gene regulates energy metabolism via the AMPK signaling pathway, increasing the levels of glycolytic intermediates and markers such as nicotinamide adenine dinucleotide (NAD). Meanwhile, L-lactate dehydrogenase (LDHB) enhances the glycolytic process under hypoxic conditions through the HIF-1 signaling pathway, catalyzing the conversion between lactate and pyruvate in muscle tissue to produce energy, thereby supporting energy supply under high-altitude hypoxia. Additionally, the GSTA1 gene improves detoxification capability and antioxidant responses through the drug metabolism-other enzymes system, alleviating oxidative stress damage. This study systematically elucidates the molecular regulatory network underlying high-altitude adaptation in Bayinbuluke sheep, providing a theoretical foundation for enhancing the genetic adaptability of livestock resources in high-altitude environments. - Source: PubMed
Publication date: 2025/11/07
Akhmiyati Par ArshatiChen BinYang YalingLiu LinglingLiu Wujun