PTGER3 antibody - C-terminal region (ARP34104_T100)
- Known as:
- PTGER3 (anti-) - C-terminal region (ARP34104_T100)
- Catalog number:
- arp34104_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PTGER3 antibody - C-terminal region (ARP34104_T100)
Related genes to: PTGER3 antibody - C-terminal region (ARP34104_T100)
- Gene:
- PTGER3 NIH gene
- Name:
- prostaglandin E receptor 3
- Previous symbol:
- -
- Synonyms:
- EP3
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2016-10-05
Related products to: PTGER3 antibody - C-terminal region (ARP34104_T100)
Related articles to: PTGER3 antibody - C-terminal region (ARP34104_T100)
- In this issue of Cancer Cell, Ma et al. identify a neoadjuvant chemotherapy-induced population of PTGER3 cancer-associated fibroblasts (CAFs) in patients with bladder cancer. These CAFs undergo lipid oxidation reprogramming and enhance CD8 T cell function, facilitating tumor microenvironment remodeling and restraining tumor progression. - Source: PubMed
Publication date: 2026/03/05
Mahadevan Krishnan KKalluri Raghu - Renal fibrosis (RF) represents a major pathological outcome of chronic kidney disease, currently accompanied by extremely limited therapeutic strategies. To decipher key cellular and molecular drivers, we integrated single-cell and bulk transcriptomic profiles for comprehensive analysis. Based on the RF-related single-cell and bulk transcriptomic data, key cell subtypes were identified through Scissor analysis, custom signature matrix construction via CIBERSORTx, and Weighted Gene Co-Expression Network Analysis (WGCNA). Subsequently, key subtype-related biomarkers were identified through the expression analysis, and functional enrichment analysis for biomarkers was conducted to elucidate the potential mechanisms by which biomarkers regulate RF. Through comprehensive profiling, thick ascending limb (TAL) cells were predominant and displayed marked heterogeneity in renal fibrosis (RF), with cortical TAL (CTAL) and adaptive TAL (aTAL) identified as principal subtypes. A set of candidate biomarkers was identified. Quantitative polymerase chain reaction (qPCR) validation in mouse models confirmed aberrant expression of these biomarkers, with STAT1 and PARP8 upregulated and HS6ST2, PTGER3, and TMEM207 downregulated in RF. Furthermore, functional enrichment analyses indicated that these biomarkers were associated with pathways underlying metabolic reprogramming and immune perturbation. Our study implicates CTAL and aTAL as central cellular players in RF and identifies their associated biomarkers. These experimentally validated biomarkers provide novel targets and repurposing opportunities for RF therapeutic intervention. - Source: PubMed
Publication date: 2026/02/16
Wang HengpingZhang YuanLi JialeFu YingWang Huiyan - Triple-negative breast cancers (TNBCs) are among the most aggressive breast tumors, due not only to the absence of clinically functional biomarkers used in other molecular subtypes, but also their marked heterogeneity and pronounced migratory and invasive behavior. The search for new molecules of interest for risk prediction, diagnosis and therapy stems from the class of long non-coding RNAs (lncRNAs), which often display context-dependent ("dual") functions and tissue specificity. Among them, lncRNA LINC01133 stands out for its dysregulation across cancer, although its molecular role in TNBC remains unclear. In the present study, we used the human TNBC cell line Hs578T to generate a cell panel comprising the parental line (Hs578T_wt), the control line (Hs578T_ctr), and the LINC01133 knockout line (Hs578T_ko). Subsequently, we performed bulk RNA-Seq to identify KO-associated Differentially Expressed Genes (DEGs) using as the primary contrast. Functional interpretation was achieved by Over-Representation Analysis (ORA) using Gene Ontology. We then conducted a comparative patient-cohort analysis using TCGA-BRCA Basal-like/TNBC cases (TCGA/BRCA n = 1098; Basal-like/TNBC n = 199), classified with the AIMS algorithm, and evaluated concordance between KO-associated signatures and patient tumor expression patterns via trend-based analyses across the LINC01133 expression levels and associated genes. A total of 265 KO-dominant DEGs were identified in Hs578T_ko, reflecting transcriptional changes consistent with tumor progression, with enrichment of pathways associated with LINC01133 knockout including cell adhesion, cell-cell interactions, epithelial-mesenchymal transition (EMT), and extracellular matrix (ECM) remodeling. The main DEGs included , , , , , , , , , and with additional candidates, such as and the lncRNA gene , which have been implicated in migration/invasion, ECM remodeling, or signaling across multiple tumor contexts. Translational analyses in TCGA-BRCA basal-like tumors suggested a descriptive association in which lower LINC01133 levels were accompanied by shifts in the expression trends of genes linked to ECM/EMT programs and modulation of genes related to cell adhesion and protease inhibition. : These results suggest a transcriptional model in which LINC01133 is associated with TNBC-related gene expression programs in a concentration-dependent manner, with loss of LINC01133 being associated with a transcriptomic shift toward pro-migratory/ECM remodeling signatures. While functional validation is required to establish causality, these data support LINC01133 as a molecule of interest in breast cancer research. - Source: PubMed
Publication date: 2026/01/24
Teodoro Júnior LeandroJesus-Ferreira Henrique César deSogayar Mari CleideNishiyama-Jr Milton Yutaka - The development and progression of bladder cancer are closely linked to its complex tumor microenvironment. and (HD-SB) are commonly used as a prominent herbal pair for treating bladder cancer. However, the pharmacological targets and molecular mechanisms by which HD-SB impacts bladder cancer require further elucidation. Additionally, it remains uncertain whether this herbal pair affects the prognosis and treatment efficacy of bladder cancer. - Source: PubMed
Publication date: 2026/02/13
Liu YuanDuan LiyuanZhu MengweiZhou ZhenzhenZhao PinZhan YonghaoZhang XuepeiZhu Zhaowei - Cancer-associated fibroblasts (CAFs) are major stromal components of the tumor microenvironment, yet how their metabolic states shift during therapy and influence anti-tumor immunity remains unclear. By integrating clinical cancer samples, single-cell RNA analyses, and functional studies, we identify a chemotherapy-conditioned PTGER3 CAF subset characterized by enhanced lipid oxidation. This metabolic reprogramming strengthens antitumor immunity by promoting CD8 T cell activation and cytotoxicity through the suppression of PTEN-related signaling. Clinically, higher proportions of therapy-induced PTGER3 CAFs correlate with improved treatment responses and better patient prognosis. Together, these findings reveal a previously unrecognized stromal metabolic adaptation that supports CD8 T cell immunity and highlight CAF-driven lipid oxidation and its regulation of CD8 T cell PTEN signaling as potential avenues to enhance chemotherapy and immunotherapy efficacy. - Source: PubMed
Publication date: 2026/02/12
Ma ZikunWang YuzhaoWang WeikaiSun WanyangWang RongDing XueChen ZibinLi XiangdongLi ZhiyongYe YunlinMao YizeYin JianhuaLi GuiboHe Rong-RongLiang XiaoyuLiu Zhuowei