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  • mProX™ Human P2RX4 Stable Cell Line

    [CAT#: S01YF-1023-PY255]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:

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    Product Information

    Target Family
    Other Targets
    Target Protein Species
    Human
    Host Cell Type
    HEK293;CHO-K1;BV-2
    Target Classification
    Other Targets Drug Discovery Assays and Products
    Target Research Area
    Pain and Addiction Research
    Related Diseases
    Anxiety; Pain Disorder
    Gene ID
    Human:5025
    UniProt ID
    Human:Q99571

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    The P2RX4 gene has been identified in several studies as having potential applications in different areas. In endometrial cancer, P2RX4 is part of a cuproptosis-related gene prognostic index (CRGPI) that can estimate prognosis, immune and molecular characteristics, and treatment benefit of immunotherapy. It is associated with better overall survival, younger age, early stage, immune cell activation, high tumor mutation burden, and better response to immune checkpoint inhibitor therapy. In uveal melanoma, P2RX4 is one of the hub genes identified in a co-expressed gene network promoting CD8+ T cell infiltration. It is involved in antigen presentation and may contribute to poor prognosis. Additionally, P2RX4 has been studied in the context of chronic trigeminal neuropathic pain, where its inhibition with an HDAC5 inhibitor reverses pain-related behaviors. Overall, P2RX4 shows potential for use as a biomarker and therapeutic target in cancer and pain management.

    Protocols

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    FAQ

    chat Jordan Miller (Verified Customer)

    Does P2RX4 play a role in Alzheimer's disease? Apr 11 2023

    chat Patrick Liam (Creative Biolabs Scientific Support)

    P2RX4 receptors in microglia contribute to memory deficits in Alzheimer's disease by promoting lysosomal ApoE degradation, which indirectly affects Aβ peptide clearance and synaptic functions. Apr 11 2023

    chat Taylor Brown (Verified Customer)

    Can P2RX4 receptors influence brain necrosis and memory disorders? Aug 19 2020

    chat Patrick Liam (Creative Biolabs Scientific Support)

    Elevated levels of lysophosphatidylcholine (LPC) can promote radiation brain necrosis and working memory disorders through P2RX4 activation, suggesting a role in radiation therapy-induced complications. Aug 19 2020

    Published Data

    Fig.1 Knockdown p2rx4 in BV-2 cells.

    In the transfection process, a reduction in P2X4R expression of 68% and 62% was achieved in Microglial BV-2 cells when they were transinfected with LV-shRNA-p2rx4, as compared to cells that were not treated (NT) and those treated solely with LV.

    Ref: Khoja, Sheraz, et al. "Reduced expression of purinergic P2X4 receptors increases voluntary ethanol intake in C57BL/6J mice." Alcohol 68 (2018): 63-70.

    Pubmed: 29477921

    DOI: 10.1016/j.alcohol.2017.09.004

    Research Highlights

    Pang, Xiaoao. et al. "Coordination of Single-cell and Bulk RNA Sequencing to Construct a Cuproptosis-related Gene Prognostic Index for Endometrial Cancer Prognosis, Immune Microenvironment Infiltration, and Immunotherapy Treatment Options." Journal of Cancer, 2023.
    This article examines the concept of procrastination in relation to academic performance. It explores the various factors that contribute to procrastination and its potential impact on students' academic success. The study also investigates the coping strategies employed by students to overcome procrastination. Results suggest that procrastination is a prevalent issue among students and can have significant consequences on their academic achievements. The findings highlight the importance of addressing procrastination in educational settings and suggest potential interventions to improve academic performance.
    Pang, Xiaoao. et al. "Coordination of Single-cell and Bulk RNA Sequencing to Construct a Cuproptosis-related Gene Prognostic Index for Endometrial Cancer Prognosis, Immune Microenvironment Infiltration, and Immunotherapy Treatment Options." Journal of Cancer, 2023.
    Pubmed: 37859813   DOI: 10.7150/jca.86325

    Zhou, Chufan. et al. "The inflammatory response-related robust machine learning signature in endometrial cancer: Based on multi-cohort studies." The journal of gene medicine, 2023.
    Uterine corpus endometrial carcinoma (UCEC) is a common cancer affecting women, characterized by abnormal cell growth in the inner lining of the uterus. Inflammation is a key factor in the progression and outcomes of UCEC, thus identifying inflammatory response-related subtypes is crucial for personalized treatment. This research identified significant differences in immune response among UCEC tumors based on molecular subtypes of inflammatory response-related genes. Subtype A showed a more favorable prognosis and was more responsive to immunotherapies. Further analysis revealed subtype-specific variations in immune response and sensitivity to chemotherapy. A 12-gene signature was also identified as a prognostic marker for UCEC patients. A validated machine learning-based signature also highlighted important clinical distinctions between low and high-risk groups. These differences included increased infiltration of certain immune cells in the low-risk group. Additionally, a correlation was found between higher risk scores and certain clinical characteristics. Knockdown of the P2RX4 gene was also observed to inhibit the proliferation of UCEC cells. In conclusion, these findings have the potential to improve targeted therapy and personalized medicine in UCEC patients through the use of this developed signature as a clinical prediction index.
    Zhou, Chufan. et al. "The inflammatory response-related robust machine learning signature in endometrial cancer: Based on multi-cohort studies." The journal of gene medicine, 2023.
    Pubmed: 37845174   DOI: 10.1002/jgm.3603

    Please note: All products are "FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR CLINICAL PROCEDURES" For licensing inquiries, please contact
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