P2RX4 antibody (FITC)
- Known as:
- P2RX4 (anti-) (fluorecein)
- Catalog number:
- orb103163
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- P2RX4 antibody (FITC)
Related genes to: P2RX4 antibody (FITC)
- Gene:
- P2RX4 NIH gene
- Name:
- purinergic receptor P2X 4
- Previous symbol:
- -
- Synonyms:
- P2X4
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2016-10-05
Related products to: P2RX4 antibody (FITC)
Related articles to: P2RX4 antibody (FITC)
- Pathological ventricular remodeling is an adverse tissue response following acute myocardial infarction (AMI), characterized by an exaggerated fibrosis leading to tissue disorganization and chronic heart failure. Cardiac fibroblasts have a prominent role in the healing process, but also in the fibrosis development, through their differentiation into myofibroblasts, which produce the extracellular matrix, in response to ischemia-reperfusion. Recently, the ATP-gated P2X4 ionotropic receptor has been identified as a key regulator of macro-autophagy, activated under metabolic challenges. - Source: PubMed
Publication date: 2026/07/10
Vinhais da Silva Ana ValeriaStrella JulietteChesseron SimonAupart ArthurHeraud-Meley AudreyMiquelestorena-Standley ElodieOhresser MarcCongiu LudovicaBoué-Grabot EricBourguignon ThierryRoger SébastienChadet StephanieIvanes Fabrice - Identifying disease-modifying drug targets is crucial for developing effective Alzheimer's disease (AD) treatments. - Source: PubMed
Publication date: 2026/06/29
Yang YuxinXu JielinHou YuanZhou YadiSaykin Andrew JCheng Feixiong - Osteoarthritis (OA) and major depressive disorder (MDD) share inflammatory and oxidative stress pathways, but the role of programmed cell death (PCD) in their comorbidity remains unclear. This study used independent OA synovial and MDD peripheral blood transcriptomic datasets-not a unified comorbid discovery cohort-to identify candidate PCD-related molecular signatures commonly dysregulated in both conditions. Transcriptomic data from OA synovium and MDD brain tissues were obtained from GEO (six training [three OA synovial and three MDD peripheral-blood], seven validation, and two single-cell RNA-seq datasets). Differentially expressed genes (DEGs) were identified, and PCD-related DEGs were screened. Machine learning (LASSO, SVM-RFE, Random Forest) was used to identify hub PCD-DEGs from the OA training set. WGCNA identified MDD-associated modules for comorbidity-gene selection. Functional enrichment, immune infiltration, scRNA-seq localization, and clinical validation (qRT-PCR/WB) were performed. From the OA cohort, four hub PCD-DEGs (CDKN1A, CX3CR1, INHBB, RHOB) showed moderate diagnostic value for OA (nomogram AUC = 0.82). Eight candidate genes (VAMP8, PDK4, P2RX4, ITM2C, IL10RA, HSP90AA1, CTSO, CRIP1) were commonly dysregulated across both OA and MDD datasets. Immune infiltration revealed upregulated B memory cells, plasma cells, Tregs, and neutrophils in OA, and neutrophils in MDD. scRNA-seq localized CDKN1A/RHOB to OA synovial cells and HSP90AA1/ITM2C to MDD neurons. Enrichment analyses highlighted TNF signaling, apoptosis, and stress responses in both diseases. An independent OA-MDD clinical cohort confirmed differential expression of CDKN1A, RHOB, ITM2C, and HSP90AA1. This study identifies four PCD-related hub genes associated with OA and eight candidate comorbidity genes showing common dysregulation across OA and MDD datasets and in an independent clinical cohort. These findings generate hypotheses about shared inflammatory pathways linking OA and MDD. As these associations derive from independent disease-specific cohorts rather than a true comorbid discovery cohort, they represent candidate signatures requiring functional validation rather than established mechanisms. - Source: PubMed
Publication date: 2026/06/06
Liu JihuaHu ZehaoXu ZixuanXiao TaoHuang QiuxuanLiu LiangjiWu Zenan - Recently, we suggested the combination of chemotherapy and P2RX4 inhibition as a promising novel therapeutic approach for P2RX4-expressing epithelial tumors to prevent paracrine resistance. Here, we aimed to assess whether determining P2RX4 expression status in colorectal and pancreatic cancer patients would allow stratification of potentially responsive patients. Therefore, P2RX4 expression levels were determined by RNA sequencing and immunohistochemistry. Subcellular localization of P2RX4 isoforms was analyzed in HeLa cells and patient-derived tumor organoids. In contrast to its RNA expression profile, P2RX4 protein levels exhibited differential regulation in human colorectal and pancreatic cancer epithelia due to alternative splicing. Interpatient heterogeneity was greater in colorectal cancer than in pancreatic cancer. Notably, these variations in expression did not correlate with overall patient survival. Alternative P2RX4 transcripts gave rise to functionally distinct protein isoforms that differed in subcellular localization and total protein abundance. Only the correctly spliced, canonical P2RX4 isoform was localized to the plasma membrane and was capable of mediating downstream signaling. Accordingly, P2RX4 inhibition in combination with chemotherapy was effective exclusively in patient-derived tumor organoids expressing the canonical P2RX4 transcript. In summary, immunohistochemical, but not transcriptomic, assessment of P2RX4 expression enabled the prediction of sensitivity to combinatorial treatment and facilitated the identification of patients who may benefit from P2RX4 inhibition during chemotherapy. Given the lower degree of heterogeneity observed in pancreatic cancer, this tumor entity may represent a promising candidate for early-phase clinical evaluation of chemotherapy combined with P2RX4 inhibition. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/06/03
Steup ChristophDosch JulianDietz-Fricke ChristopherKhosraviseftejani SaraEngel EstherValk Adalbert F deMenger DominicWelker PatrickWild Peter JKennel Kilian BKantlehner MajaZiegler Paul KGreten Florian R - The objectives of this study were to develop a real-world-data (RWD) database for patients with epilepsy to provide further real-world-evidence (RWE) for monogenic genetic epilepsies; to assess the usefulness of a diagnostic algorithm in epilepsy; and to examine protein 3D structures using in silico tools to predict variant pathogenicity. - Source: PubMed
Publication date: 2026/06/01
Morris HaleyMathew ElizabethBahl ShaliniVilla-Lopez MartaMercimek-Andrews Saadet