Ask about this productRelated genes to: P2RX7 antibody
- Gene:
- P2RX7 NIH gene
- Name:
- purinergic receptor P2X 7
- Previous symbol:
- -
- Synonyms:
- P2X7, MGC20089
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2016-10-05
Related products to: P2RX7 antibody
Related articles to: P2RX7 antibody
- Rett syndrome is a neurodevelopmental disorder caused by mutations in MECP2 and is frequently associated with scoliosis; however, the molecular mechanisms linking MeCP2 dysfunction to this phenotype remain poorly understood. In this study, we identify LBX1, a gene implicated in adolescent idiopathic scoliosis, as a downstream target of MeCP2 and investigate its regulatory role in neuronal gene expression. Chromatin immunoprecipitation (ChIP) analysis demonstrated that MeCP2 binds to the promoter region of LBX1, which contains a CT-rich and highly methylated sequence, providing a favorable context for MeCP2 binding. Consistently, CRISPR/Cas9-mediated disruption of MECP2 in A172 cells resulted in a marked reduction of LBX1 expression, whereas expression of the antisense transcript LBX1-AS remained unchanged, indicating gene-specific regulation. These findings support a role for MeCP2 as a transcriptional activator of LBX1 in this context. Given the established role of LBX1 in specifying GABAergic and glutamatergic neuronal identities, we performed targeted gene expression profiling using a GABA and glutamate-related PCR array. Several neuronal genes were differentially expressed in MeCP2-deficient cells, and GABRB1 and P2RX7 were identified as LBX1-dependent downstream targets, as their expression levels were restored by ectopic expression of LBX1. Together, these findings reveal a previously unrecognized MeCP2-LBX1 regulatory axis and suggest that its disruption may contribute to altered neuronal signaling. This pathway provides a potential molecular link between MeCP2 dysfunction and scoliosis in Rett syndrome. - Source: PubMed
Publication date: 2026/04/25
Horike Shin-IchiMeguro-Horike Makiko - Liver ischemia-reperfusion injury (IRI) is a sterile inflammatory process that contributes significantly to graft rejection following liver transplantation. Although SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) is known to preserve genomic stability and restrain inflammation under oxidative stress, its immunoregulatory function in myeloid cells during liver IRI has not been elucidated. This study aimed to investigate the role and mechanism of SETDB1 in regulating macrophage-driven inflammatory responses in liver IRI. - Source: PubMed
Publication date: 2026/04/28
Song LiuBai YiSun LingjuanYi WangLan PeixiangLiu JingChen Song - The role of P2X7R in promoting inflammation during atherosclerosis is well established; however, the effects of curcumin on P2X7R-related pathways remain poorly understood. This study investigates how curcumin affects P2X7R and related targets like NOX1, MMP-3, and TGF-β in ox-LDL-treated macrophages. THP-1-derived macrophages were exposed to 50 µg/mL oxidized low-density lipoprotein (ox-LDL) for 24 h to induce foam cell formation. Oil Red O staining was employed to confirm lipid accumulation and foam cell development. To investigate the modulatory effects, cells were exposed to P2X7R antagonist (A-438079) (100 µM) and curcumin (20, 40, and 60 µg/ml). The mRNA expression levels of P2RX7, NOX1, MMP-3, and TGF-β was evaluated using quantitative real-time PCR (RT-qPCR). Treatment induced macrophages with curcumin significantly reduced foam cell foemation, in a dose-dependent manner (P < 0.01). The mRNA expression levels of P2RX7, NOX1, MMP-3, and TGF-β were markedly upregulated in ox-LDL-treated macrophages compared to control, but significantly downregulated after treatment with curcumin (P < 0.05, P < 0.01). Similarly, treatment with selective P2X7R antagonist reduced foam cell foemation and suppressed the expression of NOX1, MMP-3, and TGF-β, thereby confirming the critical role of P2X7R in the atherogenic process development. Collectively, The present study demonstrates that curcumin exerts its anti-atherosclerotic effects primarily by inhibiting the P2X7R-mediated inflammatory pathway in ox-LDL-treated macrophages. These findings underscore curcumin's promising therapeutic potential as a natural agent for the prevention and treatment of atherosclerosis, warranting further investigation in preclinical and clinical settings. - Source: PubMed
Publication date: 2026/04/21
Samemaleki SaharAsghariazar VahidMoosavi Zenooz AliTeymuri AlirezaEterafi MajidMoini Jazani ArezooArabzadeh AmirAhmadSafarzadeh Elham - Adoptive T cell therapy (ACT) remains limited in solid tumors by poor T cell persistence within the metabolically hostile tumor microenvironment (TME). Although IL-9-producing CD8 T cells (Tc9) consistently demonstrate superior antitumor efficacy compared with conventional Tc1 cells, the selective pressures that shape their functional advantage remain unclear. Here, we show that effective ACT-mediated tumor control is accompanied by a marked increase in intratumoral extracellular ATP (eATP), representing a common metabolic consequence of tumor cell destruction. Despite comparable ATP accumulation following Tc1 or Tc9 treatment, these subsets exhibit strikingly distinct responses to ATP stress. Tc1 cells are highly susceptible to ATP-induced apoptosis, whereas Tc9 cells display intrinsic resistance, resulting in superior in vivo persistence. Mechanistically, Tc9 cells actively convert ATP signaling into enhanced mitochondrial fitness, characterized by increased oxidative phosphorylation and spare respiratory capacity. ATP exposure further drives Tc9 cells toward a tissue-resident memory (TRM) phenotype through activation of the TGF-β signaling axis. Transcriptomic and molecular analyses reveal that purinergic signaling pathways, including elevated expression of the ATP receptor P2RX7, are intrinsically enriched in Tc9 cells and are further amplified upon ATP stimulation. Collectively, our findings identify extracellular ATP as a metabolic lineage selection signal in ACT, demonstrating that ATP stress preferentially stabilizes metabolically resilient Tc9 cells by linking purinergic sensing to mitochondrial remodeling and TRM programming, thereby providing a conceptual basis for enhancing the persistence and efficacy of engineered T cell therapies in solid tumors. - Source: PubMed
Publication date: 2026/03/31
Ren JieGong ZhengrongZhong YutongXiao RuipeiUrooj KhadijaGao YuanBi EnguangWang Handuo - Malignant tumors are the leading cause of death in individuals over 65 years old, with metastasis as the primary driver. Emerging evidence suggests that age-related metabolic changes and secreted factors increase the risk of metastasis, but the underlying mechanisms remain unclear. Here we demonstrate in mice that extracellular vesicles (EVs) from senescent hepatocytes promote metastasis across tumor types. We show that aged liver tissue exhibits elevated expression of P2X purinoceptor 7 (P2RX7), which is associated with increased EV biogenesis. We identify EV-encapsulated miRNAs (miR-25, miR-92a, miR-30c and miR-30d) that reach primary tumors through the circulation and enhance tumor invasiveness and metastatic potential. Similarly, clinical samples from older patients show reduced expression of the miRNA target genes PTEN and LATS2, as well as enhanced epithelial-mesenchymal transition in metastatic tumors. Therapeutically, targeting senescence with dasatinib and quercetin (D + Q), inhibiting P2RX7, or silencing EV-associated miRNAs considerably reduces metastasis in aged mice. Together, our study uncovers a mechanism by which senescent hepatocyte-derived EVs drive tumor metastasis during aging and highlights potential strategies to mitigate this process. - Source: PubMed
Publication date: 2026/04/06
Li HuilongZhao RuzhouWan LumingYuan YangMa EnhaoLi YingangChen ZhuangzhuangLiu BinbinSong YurongCao ZiweiJiao XinxinWang YueWu PengJin HaoLi JiatongYang XiaopanHuang LinfeiZhang YanhongYang KeHuo JiangJin HaoranZhong HuiMin MinZhang ShaohuaCao YuanLi WenlongZhang RuiWei Congwen