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  • mProX™ Human EDNRA Stable Cell Line

    [CAT#: S01YF-0923-PY64]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    GPCR Cell Lines

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    Product Information

    Target Protein
    EDNRA
    Target Family
    Endothelin Family
    Target Protein Species
    Human
    Host Cell Type
    KIM-1;KYN-2;CHO-K1;HEK293
    Target Classification
    GPCR Cell Lines
    Target Research Area
    CNS Research
    Related Diseases
    Mandibulofacial Dysostosis With Alopecia;Migraine With Or Without Aura 1
    Gene ID
    Human: 1909
    UniProt ID
    Human: P25101

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    Endothelin Receptor Type A (EDNRA) plays a pivotal role in various vascular and non-vascular diseases. Recent studies have highlighted its involvement in pathological vascular remodeling, where compounds like Andrographolide have been shown to regulate the endothelin signaling pathway by inducing EDNRA expression. Furthermore, polymorphisms in the EDNRA gene have been linked to susceptibility to large artery atherosclerotic stroke in certain populations. Additionally, the EDN1/EDNRA/β-arrestin axis has been implicated in the progression of colorectal cancer, emphasizing the significance of EDNRA in cancer research3.

    Protocols

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    FAQ

    chat Kevin (Verified Customer)

    How is EDNRA significant in vascular research? Sep 04 2023

    chat Patrick Liam (Creative Biolabs Scientific Support)

    EDNRA, or endothelin receptor type A, is a receptor for endothelins, which are potent vasoconstrictors. It has been associated with pathological vascular remodeling. For instance, andrographolide has been shown to regulate smooth muscle cell (SMC) phenotypic switching and activate the endothelin signaling pathway by inducing EDNRA expression. This suggests a potential therapeutic role for modulating EDNRA in vascular diseases. Sep 04 2023

    chat James (Verified Customer)

    What is the association between EDNRA and cancer? Aug 22 2021

    chat Patrick Liam (Creative Biolabs Scientific Support)

    EDNRA has been implicated in the progression of colorectal cancer. Elevated EDNRA expression levels have been observed in colorectal cancer tissues, and its antagonism has shown potential in suppressing tumor growth and migration. This highlights the importance of the endothelin signaling pathway in tumorigenesis and offers potential therapeutic avenues. Aug 22 2021

    Published Data

    Fig.1 Significance of EDNRA for hepatocyte function revealed by transfection with siRNA.

    In HCC cell lines KIM-1 and KYN-2, renowned for elevated EDNRA expression, the EDNRA gene underwent siRNA transfection for targeted downregulation. Remarkably, this intervention conspicuously curtailed apoptosis, as evidenced by a significant reduction (p = 4.011 × 10-6 for KIM-1).

    Ref: Arai, Eri, et al. "Epigenome mapping of human normal purified hepatocytes: personal epigenome variation and genome-epigenome correlation." Epigenomics 10.7 (2018): 955-979.

    Pubmed: 29972026

    DOI: 10.2217/epi-2017-0111

    Research Highlights

    He X, et al. "Assessment of the anti-inflammatory mechanism of quercetin 3,7-dirhamnoside using ." Chemical biology & drug design, 2023.
    Pouzolzia zeylanica (L.) Benn. is a popular Chinese herbal medicine known for its anti-inflammatory and pus-removal properties. To explore its potential anti-inflammatory mechanism, the main flavonoid component, quercetin 3,7-dirhamnoside (QDR), was extracted and purified. Through network analysis, it was predicted that QDR targets a variety of proteins involved in inflammation. Molecular docking, dynamics simulations, and in vitro experiments confirmed 342 potential QDR targets. Among these, RAC1, AKT1, NOS3, mTOR, EGFR, GRB2, and EDNRA were identified as potential targets, regulating immune response, apoptosis, and anti-inflammatory activity through pathways such as PI3K/AKT, cAMP, and Ras signaling. Additionally, molecular docking and dynamics simulations revealed strong binding abilities between QDR and AKT1, mTOR, and NOS3. In RAW264.7 macrophages, QDR effectively inhibited the expression of inducible nitric oxide synthase and pro-inflammatory cytokines induced by lipopolysaccharides, while upregulating the expression of NOS3 and regulating the levels of AKT1 and mTOR. This study provides insight into the potential anti-inflammatory mechanism of QDR and its main flavonoid compound, highlighting its potential as a therapeutic agent for inflammatory conditions.
    Pubmed: 37806949   DOI: 10.1111/cbdd.14346

    Ling W, et al. "EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone ." Cancers, 2023.
    Multiple myeloma (MM) has been shown to cause dysfunction in bone marrow (BM) mesenchymal cells and promote the growth of new blood vessels. In previous studies, it was observed that pericytes and smooth muscle cells (SMCs) detached from vessels and transformed into cancer-associated fibroblasts. In this study, the researchers focused on the role of the pericyte and SMC marker, endothelin receptor type A (EDNRA), in MM progression. They found that EDNRA expression gradually increased as the disease progressed, with high-risk MM patients showing higher levels of expression compared to low-risk patients. Furthermore, EDNRA expression was highest in focal lesions. Analysis of unexpanded BM mesenchymal cells revealed that a subset of cells with high expression of proliferation genes also expressed EDNRA. Immunohistochemistry studies showed that the number of EDNRA+ cells in the interstitial BM increased as MM progressed and these cells were mostly found in areas near the MM focal growth. These EDNRA+ cells were detached from CD34+ angiogenic cells and coexpressed the pericyte markers RGS5 and periostin. This suggests that they may have originated from pericytes or SMCs that detached from vessels. These findings introduce EDNRA as a novel microenvironmental biomarker in MM and indicate that the presence of detached EDNRA+ cells is associated with disrupted vasculature and increased angiogenesis.
    Pubmed: 37760488   DOI: 10.3390/cancers15184519

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