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InVivoMAb anti-human CD4

Research Use Only
BE0003-2
Bio X Cell
ApplicationsFlow Cytometry, ImmunoPrecipitation, Other Application
Product group Antibodies
ReactivityHuman
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Overview

  • Supplier
    Bio X Cell
  • Product Name
    InVivoMAb anti-human CD4
  • Delivery Days Customer
    7
  • Applications
    Flow Cytometry, ImmunoPrecipitation, Other Application
  • Certification
    Research Use Only
  • Clonality
    Monoclonal
  • Clone ID
    OKT-4
  • Concentration
    4-11 mg/ml
  • Estimated Purity
    >95%
  • Host
    Mouse
  • Isotype
    IgG2b
  • Scientific Description
    The OKT-4 monoclonal antibody reacts with the human CD4. The CD4 antigen is a 55 kDa cell surface type I membrane glycoprotein belonging to the immunoglobulin superfamily. CD4 acts as a co-receptor which in cooperation with the T cell receptor (TCR) interacts with class II MHC molecules displayed by antigen presenting cells (APC). CD4 is expressed by the majority of thymocytes, most helper T cells, a subset of NK-T cells and weakly by dendritic cells and macrophages. CD4 plays an important role in the development of T cells and is required for mature T cells to function optimally.
  • Reactivity
    Human
  • Storage Instruction
    2°C to 8°C
  • UNSPSC
    12352203

References

  • Human Fcgamma-receptor IIb modulates pathogen-specific versus self-reactive antibody responses in lyme arthritis. Danzer H et al., 2020 Jul 2, Elife
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  • Response to Programmed Cell Death-1 Blockade in a Murine Melanoma Syngeneic Model Requires Costimulation, CD4, and CD8 T Cells. Homet Moreno B et al., 2016 Oct, Cancer Immunol Res
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  • T cell receptor dwell times control the kinase activity of Zap70. Klammt C et al., 2015 Sep, Nat Immunol
    Read more
  • Characterization of human antiviral adaptive immune responses during hepatotropic virus infection in HLA-transgenic human immune system mice. Billerbeck E et al., 2013 Aug 15, J Immunol
    Read more
  • Antibody-mediated stripping of CD4 from lymphocyte cell surface in patients with rheumatoid arthritis. Hepburn TW et al., 2003 Jan, Rheumatology (Oxford)
    Read more

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