P2RX2 antibody - N-terminal region (ARP35435_T100)
- Known as:
- P2RX2 (anti-) - N-terminal region (ARP35435_T100)
- Catalog number:
- arp35435_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- P2RX2 antibody - N-terminal region (ARP35435_T100)
Related genes to: P2RX2 antibody - N-terminal region (ARP35435_T100)
- Gene:
- P2RX2 NIH gene
- Name:
- purinergic receptor P2X 2
- Previous symbol:
- DFNA41
- Synonyms:
- P2X2
- Chromosome:
- 12q24.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-30
- Date modifiied:
- 2016-02-05
Related products to: P2RX2 antibody - N-terminal region (ARP35435_T100)
Related articles to: P2RX2 antibody - N-terminal region (ARP35435_T100)
- Source: PubMed
- Extracellular adenosine 5'-triphosphate (ATP) activates P2X receptor channels (P2XRs) that serve important roles in the immune and nervous systems. Available structures of P2XRs in detergents reveal that ATP binding to the extracellular domain leads to severing of subunit interfaces within transmembrane regions as the pore opens. Here we report cryo-electron microscopy structures of the human P2X2R in lipid nanodiscs in an apo closed state, with ATP, Mg-ATP, and suramin bound. We find that a unique Arg residue interacts with the γ-PO of ATP in P2X2R and underlies the requirement of this subtype for ATP. Channel opening and desensitization occur when ATP binds, whereas the channel remains closed when Mg-ATP binds. A continuous belt of partially resolved lipids in the outer leaflet stabilizes the closed state, and the presence of lipids prevents the severing of subunit interfaces as the channel opens. These findings establish key mechanistic principles of gating for P2X2R in a membrane-like environment, providing a framework for future mechanistic studies and therapeutic development. - Source: PubMed
Publication date: 2026/05/27
Dhingra SurbhiMoog MaiaSwartz Kenton J - Activating mutations in the epidermal growth factor receptor () gene drive non-small cell lung cancer (NSCLC). Oncogenic EGFR mutants are ligand-independent and more stable, but the underlying mechanism remains unclear. We hypothesized that EGFR mutants selectively leverage cellular stabilizers to evade degradation. Genome-wide RNA interference screens identified genes (encoding for stabilizers) responsible for mutant EGFR stability, with P2Y2 receptor (P2Y2) emerging as a bona fide stabilizer. Mechanistically, high extracellular adenosine triphosphate (ATP) levels transactivate EGFR mutants via P2Y2 activation, previously shown to signal through Src kinase-dependent EGFR phosphorylation. Our study reveals that ATP-driven P2Y2 activation stabilizes EGFR mutants by forming a P2Y2-integrin β1-EGFR complex enriched in endosomes. Targeting this axis destabilizes EGFR mutants and offers a strategy against drug resistance. Elevated P2Y2 and integrin β1 expression in patients with NSCLC implies clinical relevance. Our results provide previously unidentified insight that EGFR mutants enhance extracellular ATP levels to activate P2Y2-integrin for enhanced stability of EGFR mutants to drive the oncogenic program. - Source: PubMed
Publication date: 2026/01/21
Du YafeiWang WenjingGoh Hui ChinVaiyapuri Thamil SelvanRaju AnandhkumarHsiao Yu-ChunWang Cheng ChunAgrawal VanishaMohideen Noorul FarzanaMohd Mazian Norhidayah BinteKaratekin FerideWang Wendy KehanLakshmanan ManikandanGupta KomalChang HanLe Guezennec XavierBard FredericTan Daniel S WTergaonkar VinayHung Mien-ChieLiu XiaogangHong WanjinBoopathy Gandhi T K - Gastric cancer (GC) prevention and treatment have always been a difficult problem to solve. Therefore, mining the molecular genes related to the progression of GC and predicting the progression of GC has important clinical significance. Therefore, this study investigated whether the P2Y2 receptor (P2Y2R) has a certain effect on GC. - Source: PubMed
Publication date: 2025/12/16
Wu Yu-QingWang Wen-Long - While the etiology of Meniere's disease (MD) is likely multifactorial, genetics are thought to play a role. Several previous studies have yielded inconclusive results, potentially due to phenotypic uncertainty and variable diagnostic criteria. To explore potential genetic bases in a more rigorous context, we assessed the clinical predictors and diagnostic yield of current hearing loss panels in a highly curated cohort of patients with bilateral and/or early-onset MD. - Source: PubMed
Publication date: 2025/12/09
Shah Keshav VJung ChristianTalian DanielDavis SherrieEpstein Douglas JRuckenstein Michael JHwa Tiffany P