Ask about this productRelated genes to: SOAT1 antibody
- Gene:
- SOAT1 NIH gene
- Name:
- sterol O-acyltransferase 1
- Previous symbol:
- SOAT, STAT
- Synonyms:
- ACAT
- Chromosome:
- 1q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-04
- Date modifiied:
- 2016-10-05
Related products to: SOAT1 antibody
Related articles to: SOAT1 antibody
- Efficient lipid mobilization from yolk is critical for avian embryonic development, yet the cellular mechanisms governing lipoprotein transport in yolk sac membrane endodermal epithelial cells remain poorly characterized. Single-cell RNA sequencing was performed on 9,037 embryonic day 4 and 6,884 embryonic day 7 chicken yolk sac membrane cells to investigate lipoprotein biosynthesis pathways. Analysis identified 17 transcriptionally distinct clusters, including 3 endodermal epithelial cell subtypes. Cluster 2, characterized by high expression of epithelial markers (CDH1, EPCAM) and HDL biosynthesis genes (APOA1, ABCA1, LCAT), emerged as the primary site of HDL assembly. Apolipoprotein A1 ranked third in expression whereas apolipoprotein B ranked only 63rd, indicating a prominent HDL-biogenesis program in EECs. Gene ontology enrichment revealed upregulation of cholesterol metabolism and lipoprotein particle receptor binding pathways from embryonic day 4 to 7. Temporal expression analysis demonstrated progressive increases in HDL-related genes (APOA1, ABCA1, LCAT, SOAT1) throughout incubation, peaking at embryonic day 20, while VLDL-related genes (APOB, MTTP, SAR1B) showed sustained upregulation. Plasma analysis at embryonic day 19 confirmed HDL concentration (194.78 ± 30.13 mg/mL, mean ± SEM) significantly exceeded VLDL concentration (65.43 ± 13.82 mg/mL; P < 0.01), representing approximately 75% of measured lipoproteins. These findings reveal that HDL, rather than VLDL alone, plays a substantial role in lipid redistribution during late chicken embryogenesis, with HDL serving as the primary carrier of cholesteryl esters and phospholipids while VLDL remains the dominant triacylglycerol transporter, highlighting complementary lipoprotein functions and species-specific metabolic adaptations critical for embryonic development. - Source: PubMed
Publication date: 2026/04/17
Wu Jie-CiHu Zhao-QiLin Yuan-YuMersmann Harry JDing Shih-Torng - Macrophage polarization correlates strongly with the progression and prognosis of spinal cord injury (SCI), yet the therapeutic potential of macrophage polarization-related genes (MPRGs) in SCI remains unexplored. This study identified hub genes associated with MPRGs for SCI diagnosis, prognosis, and therapy. Differentially expressed genes (DEGs) between SCI and control groups were intersected with MPRGs to identify six differentially expressed MPRGs (DE-MPRGs). Machine learning algorithms, including LASSO, RF, and XGBoost, selected three hub genes (Soat1, Comt, and Myo1f) with elevated expression in SCI samples. Functional enrichment analysis indicated involvement in immune-related pathways. Immune infiltration analysis revealed differences in 11 immune gene sets between SCI and controls, all positively correlated with the hub genes. In silico drug prediction identified 37 small molecules, including dexamethasone and atorvastatin, as potential modulators of macrophage polarization in SCI. Single-cell RNA sequencing showed significantly higher expression of all hub genes in M2 than in M1 macrophages. RT-qPCR validation confirmed upregulation of the hub genes in SCI models. These results highlight Soat1, Comt, and Myo1f as novel hub genes in SCI, offering insights into macrophage polarization mechanisms and potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/04
Zha XiaoweiCao Shen - Inhalational exposure to polyhexamethylene guanidine (PHMG), a common disinfectant, poses major public health risks, causing severe and often fatal pulmonary fibrosis with no specific treatment available. Our prior research has demonstrated that when C57BL/6J mice are exposed to PHMG via a whole-body exposure system equipped with an ultrasonic nebulizer (3 weeks of exposure followed by a 3-week recovery period), PHMG induces pulmonary fibrosis in the mice. A key pathological feature accompanies this process: the accumulation of foam cells derived from alveolar macrophages. However, the underlying molecular mechanism driving foam cell formation remains unclear. In this study, we identified sterol O-acyltransferase 1 (SOAT1) as a critical mediator of PHMG-induced lung injury for the first time-this role had not been recognized before. Using in vivo (PHMG-exposed mice) and in vitro (lipid-loaded macrophage) models, we found PHMG exposure significantly upregulates SOAT1 in alveolar macrophages, directly disrupting cholesterol homeostasis and blocking lipophagy. This leads to excessive cholesteryl ester accumulation, promoting pro-fibrotic foam cell formation. These foam cells then secrete factors like TGF-β to activate fibroblasts. Our results confirm SOAT1 as a novel target for PHMG-induced pulmonary fibrosis. Notably, avasimibe, a selective SOAT1 inhibitor with confirmed safety, exerts multiple therapeutic effects in preclinical models. Given the growing global PHMG market and persistent human exposure risks, inhibiting SOAT1 is a feasible "drug repurposing" strategy. Additionally, SOAT1-mediated lipid dysregulation may offer a new therapeutic direction for other lipid metabolism-related fibrotic lung diseases. - Source: PubMed
Publication date: 2026/04/21
Ding YuchaoWang SiqiSun HeYan ZhijiaoSun JiaxingGuo CaihongWang HongmeiTang JinglongJi XiaoyaTian ShuhanRen Dunqiang - Cholesterol esterification is a fundamental step in cholesterol metabolism and transport, and in humans, it is operated by three enzymes. Lecithin:cholesterol acyltransferase (LCAT) is responsible of cholesterol esterification in plasma and other biological fluids including cerebrospinal fluid (CSF), where it is mainly activated by apolipoprotein E. Esterification of cholesterol within cells is instead operated by sterol O-1 and O-2 acyltransferases (SOAT1 and SOAT2). SOAT1 is expressed in all cell types, while SOAT2 is expressed in hepatocytes and enterocytes, where it produces cholesteryl esters (CEs) to be assembled within VLDL and chylomicrons. LCAT and SOAT1/2 have different substrate specificity; LCAT has a preference for the unsaturated fatty acids, while the SOAT enzymes prefer the saturated (SFAs) and monounsaturated fatty acids (MUFAs). Here, we show that CSF CEs have a different composition compared to plasma CEs and specifically are more enriched in SFAs and MUFAs, typical substrates of the SOAT2 enzyme, and less frequently used by LCAT. Protein and RNA analysis in astrocytes, the main lipoprotein-producing cells in the central nervous system, excluded the presence of SOAT2, thus suggesting that CSF CEs are products of the LCAT enzyme. In line with this hypothesis, CSF phosphatidylcholine, the substrate of LCAT, is enriched in SFAs and MUFAs and depleted in polyunsaturated fatty acids. Moreover, we show that in Alzheimer's disease patients, CSF CEs are enriched in SFA, thus adding new insights into our recent observation that LCAT-mediated cholesterol esterification is hampered in Alzheimer's disease. In conclusion, the present findings not only clarify the enzymatic origin of CSF CEs but also open avenues for developing enzyme-specific biomarkers and therapeutic strategies aimed at restoring lipid homeostasis in the brain. - Source: PubMed
Publication date: 2026/04/03
Pavanello ChiaraOssoli AliceComi ChiaraTurri MartaTremolizzo LucioConti ElisaD'Incecco PaoloBarbiroli AlbertoParini PaoloMitro NicoCaruso DonatellaSierri GiuliaRe FrancescaChinello CliziaFumagalli ClaudiaMagni FulvioFernandes KarlCalabresi Laura - To construct and validate a diagnostic model for osteonecrosis of the femoral head (ONFH) based on alcohol exposure-related genes using machine learning methods. - Source: PubMed
Tao HongchengLiang FukaiHuang WenboFan SiqiZeng Ping