Ask about this productRelated genes to: TBXAS1 antibody
- Gene:
- TBXAS1 NIH gene
- Name:
- thromboxane A synthase 1
- Previous symbol:
- -
- Synonyms:
- CYP5, CYP5A1, THAS, TXS, TXAS, TS
- Chromosome:
- 7q34
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-07
- Date modifiied:
- 2019-04-23
Related products to: TBXAS1 antibody
Related articles to: TBXAS1 antibody
- This work aimed to identify candidate renin-angiotensin system (RAS)-related blood transcriptomic biomarkers associated with hypertension, construct an externally tested candidate diagnostic model, and validate selected genes in an Ang II-induced endothelial cell model. Two public microarray datasets, GSE75360 and GSE74144, were analyzed. Differential expression analysis was performed using limma, followed by GO/KEGG enrichment, preranked GSEA, CIBERSORT immune infiltration analysis, protein-protein interaction and regulatory network construction, and machine learning-based feature selection using logistic regression and random forest. A logistic regression model based on the selected genes was developed in GSE75360 and externally tested in GSE74144. Experimental validation was performed in Ang II-induced HUVECs using qRT-PCR, western blotting, ELISA, and CST3/FURIN loss- and gain-of-function assays, followed by CCK-8, Transwell, inflammatory, oxidative stress, and endothelial function analyses. In GSE75360, 173 differentially expressed genes were identified, including 18 RAS-related differentially expressed genes. Eight candidate genes, LRP1, CTSD, MTHFR, AUTS2, FURIN, CST3, FCER1G, and TBXAS1, were selected by combined machine learning analyses. Enrichment and immune infiltration analyses indicated that these genes were mainly associated with immune and inflammatory signatures. The eight-gene model showed high discrimination in GSE75360 and retained moderate performance in GSE74144. In Ang II-treated HUVECs, most candidate genes were upregulated at the mRNA level, and CST3, FURIN, and TBXAS1 were further validated at the protein level. CST3 and FURIN modulation altered Ang II-induced endothelial viability, migration, expression of inflammatory/adhesion markers, ROS accumulation, and eNOS/NO-related functional readouts. This study identified candidate RAS-related biomarkers and immune-associated signatures in hypertension and developed an externally tested candidate diagnostic model. The in vitro findings support the functional relevance of CST3 and FURIN in Ang II-induced endothelial responses, warranting further clinical and mechanistic validation. - Source: PubMed
Publication date: 2026/06/22
Bai JingWang YanYang XiangxiangDu LiShi JianhuaLi XiaxiaBai Ming - Microglia accumulate in malignant gliomas and play a pivotal role in tumor progression. Using single‑cell RNA sequencing studies researchers have probed gene expression in the myeloid cells in experimental gliomas at relatively late stages of the tumor development. Therefore, the early changes in gene expression in microglia in response to glioma are not fully characterized. We have previously reported distinct profiles of gene expression in the rat primary microglia cultures treated for 6 hours with either rat C6 glioma‑conditioned medium (GCM) or lipopolysaccharide. In the current study, using RNA‑seq, we characterized the transcriptional response of rat primary microglia to GCM in vitro at different time‑points: 6 h, 24 h, and 48 h, as compared to the control treated for 6 h with its own medium. We observed that during the GCM treatment gene expression changes in a biphasic, swing‑like pattern. This includes the genes involved in innate immune response, which are mostly down‑regulated at 6 h by the GCM treatment, as compared to the time‑matched control, and subsequently up‑regulated at 48 h, as compared to the earlier time‑points of the GCM treatment. Conversely, the genes involved in the cell cycle are up‑regulated at 6 h and down‑regulated at 48 h, which coincides with the induction of Tgfb1. Notable exceptions to this biphasic pattern include key genes activating immune response, such as Tlr9 and Myd88, which are down‑regulated early and persistently, while genes inhibiting immune activation, such as Trem1, and genes involved in a metabolic switch, such as Pfkl, are persistently up‑regulated. Most notably, the up‑regulated genes include Ptgs1 (alias Cox1) and Tbxas1, which encode the enzymes catalyzing the synthesis of thromboxane A2, a known inducer of T cell suppression. Further studies are needed to test the functional consequences of their up‑regulation. - Source: PubMed
Publication date: 2026/04/27
Dąbrowski MichałKaza BeataGielniewski BartłomiejWojtaś BartoszKamińska BożenaMaleszewska Marta - Parkinson's disease (PD) is a prevalent neurodegenerative disorder for which reliable biomarkers are needed to facilitate early detection and the development of targeted therapeutic strategies. Neuroinflammation has emerged as a key feature in both the initiation and progression of PD, yet the underlying regulatory networks remain incompletely understood. In this study, we integrated single-cell RNA sequencing (scRNA-seq) with bulk transcriptomic data and weighted gene co-expression network analysis (WGCNA) to identify inflammation-associated genes in PD. A PD risk score was constructed using logistic regression and LASSO, and potential functional mechanisms were explored through gene enrichment analyses. Candidate biomarker was further evaluated using in vitro cell assays and peripheral blood samples from PD patients. Our results revealed that the inflammation levels increase dynamically with disease progression and were closely associated with alterations in cellular composition. Microglia appeared to be central contributor to the inflammatory microenvironment. Among the identified genes, TBXAS1 was found to influence neuronal proliferation and apoptosis, potentially through the regulation of pro-inflammatory factor secretion in microglia. Collectively, these findings suggested that TBXAS1 may represent a candidate biomarker and potential microglia-associated inflammatory regulator in PD, providing a theoretical foundation for future studies on risk prediction and therapeutic intervention. - Source: PubMed
Publication date: 2026/06/13
Guan XiaoxueZhao QiangDeng YongLu Zuneng - This study investigates the molecular mechanisms underlying bisphenol A (BPA)-induced clear cell renal cell carcinoma (ccRCC). We integrated transcriptomic data from multiple GEO datasets and performed differential expression analysis and WGCNA to identify BPA-associated candidate genes. Enrichment analyses implicated pathways including cell adhesion, lipid metabolism, arachidonic acid signaling, and innate immune response. Using twelve machine learning algorithms, we identified four core genes (ITGB2, TBXAS1, LIPA, and CLEC7A), all upregulated in ccRCC. Molecular docking suggested stable BPA-protein interactions with favorable binding energies. Single-cell analysis showed predominant expression of these genes in monocytes and macrophages. LIPA was elevated in kidney cancer tissues and associated with clinical outcomes. In vitro experiments confirmed that BPA exposure promoted ccRCC cell progression by regulating core gene expression. This integrated approach offers new insights into the molecular mechanisms of BPA-induced ccRCC and identifies potential biomarkers for environmental risk assessment. - Source: PubMed
Publication date: 2026/05/25
Chen JianyuWu LianquanJin HaoqiLi Yeping - Arachidonic acid (AA), a membrane-abundant polyunsaturated fatty acid, is primarily liberated from membrane phospholipids by phospholipase A (PLA), and is subsequently metabolized into bioactive eicosanoids involved in vascular tone and inflammation. With lipidomics advances, AA metabolism's multifaceted roles in the tumor microenvironment (TME) have emerged, and it is recognized as a key driver and potential therapeutic axis in lung adenocarcinoma (LUAD). We utilized spatial transcriptomics sequencing (ST-seq) and LUAD-associated single-cell RNA sequencing (scRNA-seq) to explore crucial AA-related biomarkers in LUAD. - Source: PubMed
Publication date: 2026/05/19
Sun ChongqiZhang YuchenPan YunXia GuixiYang GuangrongHuang ChunkaiLi JunMa Pei