Ask about this productRelated genes to: P2RX5 antibody
- Gene:
- P2RX5 NIH gene
- Name:
- purinergic receptor P2X 5
- Previous symbol:
- -
- Synonyms:
- P2X5, LRH-1
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-14
- Date modifiied:
- 2016-10-05
Related products to: P2RX5 antibody
Related articles to: P2RX5 antibody
- This study aims to investigate the impact of P2RX5 on the clinical pathological characteristics and prognosis of endometrial carcinoma, and to explore its potential underlying mechanisms. - Source: PubMed
Publication date: 2026/03/15
Huang Li-YanSu Qun-YingLong Qin-QinTian Feng-QinZhu Xiao-YingLong Xi-Dai - While CD19- and BCMA-directed immunotherapies have improved outcomes for B-lymphoid and plasma cell malignancies, frequent relapses with antigen loss/downregulation highlight the need for new targets. Here, using transcriptomic datasets and newly-developed monoclonal antibodies, we show that , long considered a pseudogene in humans, encodes a stable protein in 80% of individuals of African descent carrying the ancestral haplotype. Like CD19, P2RX5 displays B-cell lineage-restricted expression in normal tissues. Unlike CD19, P2RX5 is expressed not only in B-cell neoplasms, but also in T-cell leukemia (T-ALL) and multiple myeloma (MM). We developed P2RX5-directed bispecific T-cell engagers and CAR T cells, which killed T-ALL cells with no evidence of T-cell fratricide. These agents were non-inferior to FDA-approved CD19- and BCMA-directed immunotherapeutics in cell culture and xenograft models of Burkitt lymphoma and MM, while maintaining potency against CD19- and BCMA-negative variants. Hence, P2RX5 is a unique multi-lineage target for frontline or salvage immunotherapy. - Source: PubMed
Publication date: 2026/01/26
Ang ZhiweiCastro AnnetteParuzzo LucaSchimdt CarolinHasanali Zainul SHayer Katharina EStella FedericoSoldan Samantha STorres-Diz ManuelKwok ChristopherSainos Patricia KingJi KaylaKrohl Patrick JFine JustynSehgal PriyankaMartinez DanielSpangler Jamie BRiley James LVogl Dan TPorazzi PatriziaPillai VinodhLieberman Paul MAllman DavidRuella MarcoThomas-Tikhonenko Andrei - Driven by the demand for sustainable, safe, and cost-effective medical materials, design of biodegradable metals increasingly aims to achieve higher strength and biofunctionality with less alloying. This study proposes a high strengthening-efficiency (high-SE) design strategy and develops novel Zn-0.8Mn-0.1Mg and Zn-0.8Mn-0.1Li alloys. With total alloying additions below 1 wt.%, these alloys achieve yield strength of 369-397 MPa, elongation of 42-57%, and remarkable strengthening efficiency (SE) of 6.4-6.8. These SE values represent the highest level among high strength-ductile Zn alloys (YS > 300 MPa, EL > 40%). Benefiting from the synergistic release of Zn, Mn, and Li/Mg ions, both the alloys exhibit superior antibacterial activity, cytocompatibility, controlled degradation rates, and in vivo osteogenesis, demonstrating excellent degradation-osteogenesis coupling effect. Notably, Zn-0.8Mn-0.1Mg further enhances osteogenesis by activating the PI3K/Akt/HIF-1α signaling axis, which coordinates cascades of immunomodulation (e.g., IGF2, P2rx5), anti-inflammation (e.g., Nfkbia inhibition), and cellular energy metabolism (e.g., Ndufaf3), resulting in a more pronounced osteogenic effect. This work establishes a new paradigm for high-efficiency alloy design, achieving simultaneous breakthroughs in mechanical and biofunctionality, offering a promising framework for next-generation Zn-based orthopedic implants. - Source: PubMed
Publication date: 2025/12/16
Li Xiang-MinLiu Ding-GeYang GangShi Zhang-ZhiXin Fang-HaiWang Jia-YiWang Yi-XuanLiu Kai-PingPei YinDeng Shuang-ShuangLiu Rui-JieZhang Hai-JunZhang XinWang Lu-Ning - Establishing a comprehensive characterization of the regulatory landscapes of cattle tissues facilitates a better understanding of the biological mechanisms responsible for condition-dependent phenotypes that drive tissue-specific gene regulation, developmental processes, and responses to environmental or physiological cues. This can be achieved through the characterization of gene expression, transcript usage and open chromatin accessibility. While much of this work has been done in human and biomedical model species, there is a lack of research in cattle that jointly characterizes chromatin accessibility and transcript usage alongside gene expression to define tissue-specific regulatory landscapes in cattle. Samples of prefrontal cortex (PFC), liver (L), and skeletal muscle (SM) were collected from four 3-month-old Angus steers and subjected to ATAC-seq and RNA-seq analyses. Differential gene expression (DGE) and transcript usage (DTU) were quantified across the tissues and evaluated in PFC-L, PFC-SM, and L-SM pairwise comparisons. - Source: PubMed
Publication date: 2025/11/29
Khilji Sarem FXie ShangqianBecker Gabrielle MShira Katie AStegemiller Morgan RWoods Julia LWilliams Janet EChristensen Lauren EKonetchy Denise EHagen Darren EMurdoch Gordon KMcKay Stephanie DMurdoch Brenda M - Focal Cortical Dysplasia Type II (FCDII) is a subtype of cortical malfunction and is the primary cause of drug-resistant epilepsy in children. Although somatic mosaicism and clonal expansion of brain cells have been identified as crucial factors in FCD cases, the overall genetic landscape and clinical implications of FCDII remain largely unclear due to a significant gap in translating genetic data to inform surgical approaches and prognostic evaluations of individual cases. We carried out deep exome sequencing and deep amplicon validation of surgical biopsies and matched blood samples from 14 FCDII patients with confirmed neuropathology. We further performed multiscale pathogenic validations and took advantage of existing single-nucleus RNA sequencing and spatial maps from developing human cortices to explore the functionality of potential pathogenic somatic variants. We identified novel somatic variants in several functional categories, like neurotransmission (), structural regulation (), cellular maintenance (), and RNA processing (), mapping the expression of these genes back to the developing human brain demonstrated significant enrichment in neuronal cell types, especially excitatory neurons, further confirming their contributions in early brain development and phenotypic functions in dysmorphic neurons. Combining these genetic findings with clinical phenotypes, we found brain-specific mosaic variants with very high mosaic fractions (fraction of mosaic cells, MF, up to 99.5% on ) associated with different clinical phenotypes. FCDIIB, a more severe subtype that contains balloon cells, had higher MFs (>40%) for variants within resectable cortical layers (excitatory neurons in Layers 5 and 6). This allows potentially targeted resection and achieves better clinical outcome (87.5 % with Engel score I). FCDIIA subtype, on the other hand, displayed lower MFs (<5%) with diffuse distribution, and required hemispherectomy, with poor surgical outcomes (Engel score II/III). Our results suggest MF thresholds are high-definition biomarkers of surgical outcome estimate, with MF > 40% predicting viable focal resection and MF < 5% indicating network dysfunction that necessitates broad-spectrum resection. Combining genetic mapping with cellular localization thus offers a coherent solution to precision surgery in FCDII, translating molecular diagnosis to clinical practice. - Source: PubMed
Publication date: 2025/10/07
Bernardino Garcia Camila AraújoZubair MuhammadXi XincenGraham Ian AlfredLee Sang HyunPatarlapalli Sai BabuSantos Marcelo VolponMachado Hélio RubensYang Xiaoxu