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  • mProX™ Human THRA Stable Cell Line

    [CAT#: S01YF-1123-KX111]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    Nuclear Receptor

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    Product Information

    Target Protein
    THRA
    Target Family
    Thyroid Hormone Receptor
    Target Protein Species
    Human
    Host Cell Type
    HepG2; CHO-K1; HEK293; RL95-2; KLE
    Target Classification
    Nuclear Receptor
    Target Research Area
    Metabolic Research
    Related Diseases
    Hypothyroidism
    Gene ID
    UniProt ID

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    The THRA gene in humans codes for the nuclear receptor protein known as thyroid hormone receptor alpha (TR-alpha). This gene codes for a triiodothyronine nuclear hormone receptor protein. It has been demonstrated that this particular receptor, one of numerous for thyroid hormone, mediates the hormone's biological effects. Thyroid hormone actions may be mediated by distinct receptors, despite some redundancy, according to studies on knockout mice. There have been reports of alternatively spliced transcript variants encoding different isoforms. The customized THRA stable cell line can be used in antibody discovery and development, potential drug candidate screening and signaling pathway researches.

    Protocols

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    Customer Reviews

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    The protocol of THRA cell line was straightforward, and the results were consistent. Dec 24 2020

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    The convenience of the mouse THRA KO cell line has significantly streamlined my workflow. Nov 09 2020

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    FAQ

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    Published Data

    Fig.1 T3 represses STMN1 expression in HepG2 cell lines

    THR protein expression levels in THR overexpressing and control HepG2 cell lines. HepG2-THRA, HepG2-THRB, and HepG2-Neo cell lysates immunoblots.

    Ref: Tseng, Yi-Hsin, et al. "Thyroid hormone suppresses expression of stathmin and associated tumor growth in hepatocellular carcinoma." Scientific reports 6.1 (2016): 38756.

    Pubmed: 27934948

    DOI: 10.1038/srep38756

    Research Highlights

    THRA mutations might be more prevalent than thought. A molecular analysis of THRA abnormalities is strongly advised in patients exhibiting clinical signs of mild hypothyreosis without evidence of the condition being confirmed by endocrine studies.
    Tylki-Szymańska, Anna, et al. "Thyroid hormone resistance syndrome due to mutations in the thyroid hormone receptor α gene (THRA)." Journal of medical genetics 52.5 (2015): 312-316.
    Pubmed: 25670821   DOI: 10.1136/jmedgenet-2014-102936

    This example demonstrates that even if clinical and biological aspects are different from previously reported cases of RTHα, patients with a low FT4/FT3 ratio should be examined for THRA mutations.
    Espiard, Stéphanie, et al. "A novel mutation in THRA gene associated with an atypical phenotype of resistance to thyroid hormone." The Journal of Clinical Endocrinology & Metabolism 100.8 (2015): 2841-2848.
    Pubmed: 26037512   DOI: 10.1210/jc.2015-1120

    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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