P2RX7 _ P2X7 receptor

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Known as:: P2RX7 _ P2X7 receptor
Catalog number:: Y214268
Product Quantity:: 200ul
Category:: -
Supplier:: ABM
Gene target:: P2RX7 _ P2X7 receptor

Related genes to: P2RX7 _ P2X7 receptor

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 _ P2X7 receptor

Related articles to: P2RX7 _ P2X7 receptor

Curcumin regulates P2X7R level to inhibit TGF-β, NOX1, and MMP-3 expression in ox-LDL-treated macrophages.
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
Extracellular ATP Functions as a Metabolic Lineage Selection Signal That Stabilizes Tc9 Cells During Adoptive T Cell Therapy.
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
Extracellular vesicles derived from senescent hepatocytes drive pan-cancer metastasis in aging.
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
SETDB1 modulates neuroinflammation in the mouse cortex by regulating neuronal P2rx7 expression.
Neuroinflammation is a pivotal feature of neuropsychiatric conditions, yet the brain-intrinsic epigenetic mechanisms initiating this response are not fully understood. In this study, we show that loss of the histone H3K9me3 methyltransferase SETDB1 in excitatory neurons (Setdb1-CK-cKO) triggers endogenous retrovirus (ERV) activation and neuroinflammation in the mouse cortex. ERV activation occurs in both neurons and astrocytes, leading to the emergence of a distinct reactive astrocyte population with increased expression of inflammatory chemokines and cytokines. Mechanistically, we identify the purinergic receptor gene P2rx7 as a direct target of SETDB1. We characterize a novel enhancer in the P2rx7 first intron that is epigenetically silenced by SETDB1; loss of SETDB1 results in increased chromatin accessibility and aberrant P2rx7 overexpression. This epigenetic regulatory mechanism is conserved between mouse and human. Moreover, genetic ablation of P2rx7 in Setdb1-CK-cKO mice partially reverses ERV activation and inflammatory gene dysregulation, and attenuates synaptic dysfunction. These findings provide new mechanistic insight into the epigenetic regulation of P2X7R signaling in controlling endogenous neuroinflammatory responses in the central nervous system. - Source: PubMed
Publication date: 2026/04/04
Zhu YueyanLiao LiyongLiu XixiSheng HuanSun DaijingLi JiaqiChen QiZhang ChenchunWang ShunyingZhang YuanWeng JieZhou MenglingYang JiannengDong YuhaoPeng WenzhuLi YueJiang Yan
P2X7 receptor-mediated cGAS-STING pathway activation underlies chronic stress-induced depressive-like behaviors.
Although chronic stress is known to trigger neuroinflammation and depressive-like behaviors, the mechanisms linking stress sensors to inflammatory cascades remain elusive. The purinergic receptor P2X7 (P2X7R), an extracellular ATP-gated cation channel primarily expressed in microglia, is a critical link between stress and neuroinflammation. While the cGAS-STING signaling pathway has been implicated in microglial reactivity, it remains unknown whether P2X7R signals via this pathway. Here, we demonstrate that chronic restraint stress in mice activates microglial P2X7R in the hippocampus, inducing mitochondrial damage. This was accompanied by activation of the cGAS-STING pathway, elevating phosphorylated STING and IRF3 levels along with pro-inflammatory cytokines. Pharmacological inhibition of P2X7R (JNJ-47965567) or STING (H-151) attenuated neuroinflammation and alleviated depressive-like behaviors. In vitro, LPS-stimulated BV2 microglia exhibited mtDNA release and cGAS-STING activation. P2X7R knockdown or pharmacological inhibition attenuated mitochondrial dysfunction, mtDNA release, and subsequent phosphorylation of STING and IRF3. In conclusion, our findings unveil a previously unrecognized mechanism in the neuroimmunological pathology of depressive-like behaviors, demonstrating that chronic stress triggers neuroinflammation through a microglial pathway involving P2X7R-mediated mitochondrial damage, mtDNA release, and cGAS-STING activation. - Source: PubMed
Publication date: 2026/03/30
He Xi-MengZhang YiChen Cui-YuanTang Yu-Li HanLi Xuan

P2RX7 _ P2X7 receptor

Related genes to: P2RX7 _ P2X7 receptor

Related products to: P2RX7 _ P2X7 receptor

Related articles to: P2RX7 _ P2X7 receptor

Curcumin regulates P2X7R level to inhibit TGF-β, NOX1, and MMP-3 expression in ox-LDL-treated macrophages.

Extracellular ATP Functions as a Metabolic Lineage Selection Signal That Stabilizes Tc9 Cells During Adoptive T Cell Therapy.

Extracellular vesicles derived from senescent hepatocytes drive pan-cancer metastasis in aging.

SETDB1 modulates neuroinflammation in the mouse cortex by regulating neuronal P2rx7 expression.

P2X7 receptor-mediated cGAS-STING pathway activation underlies chronic stress-induced depressive-like behaviors.