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  • mProX™ Human IKBKB Stable Cell Line

    [CAT#: S01YF-1123-KX264]
    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-KX1169 Magic™ Human IKK-beta in Vitro Assay Human Kinase Assay

    Product Information

    Target Protein
    IKBKB
    Target Family
    Kinases/Enzyme Drug Discovery Assays and Products
    Target Protein Species
    Human
    Host Cell Type
    CHO-K1; HEK293
    Target Classification
    Kinase Cell Lines
    Target Research Area
    Immunology Research
    Related Diseases
    Immunodeficiency 15A and Immunodeficiency 15B. Among its related pathways are MyD88 dependent cascade initiated on endosome and TNFR1 Pathway
    Gene ID
    UniProt ID

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    The protein IKK-β, sometimes referred to as inhibitor of nuclear factor kappa-B kinase subunit beta, is encoded by the IKBKB gene in humans. IKK-β is an enzyme that functions as a protein subunit of IκB kinase, a part of the intracellular signaling pathway that is activated by cytokines and responsible for inducing immunological responses. Nuclear Transcription factor kappa-B, or NF-κB, is a transcription factor that is activated by IKK activity. The protein known as the inhibitor of NF-κB, or IκBα, is phosphorylated by activated IKK-β and binds to NF-κB to prevent it from functioning. The ubiquitination pathway breaks down phosphorylated IκB, releasing NF-κB and enabling its entry into the cell nucleus, where it activates several genes linked to inflammation and other immune responses. The customized IKBKB 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 William

    The IKBKB KO cell line worked as advertised and was a cost-effective alternative in our studies. Apr 08 2022

    chat Verified Customer

    chat Jessica

    The IKBKB cell line worked flawlessly, and the detailed protocols provided by the company made the whole process much easier. Aug 10 2022

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    FAQ

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

    Published Data

    Fig.1 pS13 HTT levels are regulated by inhibitor of IKBKB and okadaic acid-sensitive phosphatases.

    HEK293T cells overexpressing N571 Q55 HTT were treated with okadaic acid (OA), either in the presence or absence of IKBKB or its kinase-dead mutant IKBKB KD. When IKBKB is overexpressed in conjunction with OA therapy, Western blotting demonstrates significantly elevated pS13 HTT levels and enhanced auto-phosphorylation of IKBKB at residues S177/S181. However, IKBKB KD overexpression is not observed.

    Ref: Cariulo, Cristina, et al. "IKBKB reduces huntingtin aggregation by phosphorylating serine 13 via a non-canonical IKK pathway." Life Science Alliance 6.10 (2023).

    Pubmed: 37553253

    DOI: 10.26508/lsa.202302006

    Research Highlights

    Through downregulating IKBKB, miR-200b, a transcriptional target of NF-κB, inhibits the proliferation and migration of breast cancer cells as well as NF-κB activation. This suggests that miR-200b may have use in breast cancer patients as a therapeutic target.
    Wu, Hewen, et al. "A negative feedback loop between miR-200b and the nuclear factor-κB pathway via IKBKB/IKK-β in breast cancer cells." The FEBS journal 283.12 (2016): 2259-2271.
    Pubmed: 26433127   DOI: 10.1111/febs.13543

    This missense mutation results in very similar cellular and metabolic abnormalities in humans and mice. Precise rodent models created with CRISPR/Cas9 can provide information on pathogenesis and aid in the characterization of new syndromes resulting from de novo germline mutations.
    Cardinez, Chelisa, et al. "Gain-of-function IKBKB mutation causes human combined immune deficiency." Journal of Experimental Medicine 215.11 (2018): 2715-2724.
    Pubmed: 30337470   DOI: 10.1084/jem.20180639

    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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