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  • mProX™ Human EPHA2 Stable Cell Line

    [CAT#: S01YF-1123-KX225]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    Kinase Cell Lines

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    Host Cell Type:
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    Based on this stable cell line, we also provide cell-based in vitro assays to evaluate the effects of your compounds or antibodies.

    Sub Cat Product Name Target Protein Species Host Cell Type Assay Types Inquiry Datasheet
    S01YF-1122-KX1123 Magic™ Human EPHA2 in Vitro Assay Human Kinase Assay

    Product Information

    Target Protein
    EPHA2
    Target Family
    Kinases/Enzyme Drug Discovery Assays and Products
    Target Protein Species
    Human
    Host Cell Type
    MDA-MB-231; BT549; HCC1395; HCC1937; HCC1806; HBL-100; CHO-K1; HEK293
    Target Classification
    Kinase Cell Lines
    Target Research Area
    Ocular Research
    Related Diseases
    Cataract 6, Multiple Types and Cataract. Among its related pathways are GPCR Pathway and ERK Signaling
    Gene ID
    UniProt ID

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    The EPHA2 gene in humans encodes the protein known as EPH receptor A2 (ephrin type-A receptor 2). This gene is a member of the protein-tyrosine kinase family's ephrin receptor subfamily. Developmental events have been linked to EPH and EPH-related receptors, especially in the nervous system. The extracellular region of receptors in the EPH subfamily usually has two repeats of fibronectin type III and a Cys-rich domain, in addition to a single kinase domain. Based on the similarity of their extracellular domain sequences and their propensity to bind ephrin-A and ephrin-B ligands, the ephrin receptors are classified into two classes. A protein that binds ephrin-A ligands is encoded by this gene. The customized EPHA2 stable cell line can be used in antibody discovery and development, potential drug candidate screening and signaling pathway researches.

    Protocols

    Please visit our protocols page.

    Customer Reviews

    chat Amy

    The EPHA2 cell line design is well-optimized, and the provided documentation is comprehensive. It has saved me time and effort compared to traditional methods. Mar 02 2023

    chat Verified Customer

    chat Stephanie

    Most importantly, I would recommend this product to anyone who wants to research EPHA2. Aug 20 2023

    chat Verified Customer

    FAQ

    Any questions about our products? Please visit our frequently asked questions page.

    Published Data

    Fig.1 EphA2 knockdown impairs proliferation in human TNBC cell lines.

    Stable short hairpin RNA (shRNA) knockdown sublines were created in six different human TNBC lines in order to ascertain the function of EphA2 in TNBC. Immunoblot analysis showed that shEphA2 lines had>90% knockdown.

    Ref: Song, Wenqiang, et al. "Targeting EphA2 impairs cell cycle progression and growth of basal-like/triple-negative breast cancers." Oncogene 36.40 (2017): 5620-5630.

    Pubmed: 28581527

    DOI: 10.1038/onc.2017.170

    Research Highlights

    Additionally, this review highlights the potential and difficulties of targeting EphA2 in cancer by summarizing finished and continuing clinical trials.
    Wilson, Kalin, Eileen Shiuan, and Dana M. Brantley-Sieders. "Oncogenic functions and therapeutic targeting of EphA2 in cancer." Oncogene 40.14 (2021): 2483-2495.
    Pubmed: 33686241   DOI: 10.1038/s41388-021-01714-8

    Within the subfamily of receptor tyrosine kinases, the Eph (erythropoietin-producing human hepatocellular) receptors are the largest. Direct cell-to-cell contacts between these receptors and membrane-bound ephrin ligands cause the bidirectional activation of signal pathways.
    London, Max, and Eugenio Gallo. "The EphA2 and cancer connection: potential for immune-based interventions." Molecular Biology Reports 47 (2020): 8037-8048.
    Pubmed: 32990903   DOI: 10.1007/s11033-020-05767-y

    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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