MAb to C. trachomatis LPS

  • Catalog number
    MBS312981
  • Price
    Please ask
  • Size
    5x1 mg
  • Products_type
    Antibody
  • Products_short_name
    [Chlamydia trachomatis LPS]
  • Products_name_syn
    [MAb to C. trachomatis LPS]
  • Clonality
    Monoclonal
  • Clone
    [B1214M]
  • Specificity
    Reacts with Chlamydia trachomatis LPS.
  • Purity
    Protein A chromatography
  • Form
    Purified, Liquid; PBS, pH 7.5
  • Concentration
    4.45 mg/ml
  • Storage_stability
    Store at 2-8 degree C.
  • Tested_application
    Lateral Flow Assay
  • Gene
    Bacterial pathogen lipopolysaccharides (LPS) are the major outer surface membrane components present in almost all Gram-negative bacteria and act as extremely strong stimulators of innate or natural immunity in diverse eukaryotic species ranging from insects to humans. LPS consist of a poly- or oligosaccharide region that is anchored in the outer bacterial membrane by a specific carbohydrate lipid moiety termed lipid A. The lipid A component is the primary immunostimulatory center of LPS. With respect to immunoactivation in mammalian systems, the classical group of strongly agonistic (highly endotoxin) forms of LPS has been shown to be comprised of a rather similar set of lipid A types. In addition, several natural or derivative lipid A structures have been identified that display comparatively low or even no immunostimulation for a given mammalian species. Some members of the latter more heterogeneous group are capable of antagonizing the effects of strongly stimulatory LPS/lipid A forms. Agonistic forms of LPS or lipid A trigger numerous physiological immunostimulatory effects in mammalian organisms, but--in higher doses--can also lead to pathological reactions such as the induction of septic shock. Cells of the myeloid lineage have been shown to be the primary cellular sensors for LPS in the mammalian immune system. During the past decade, enormous progress has been obtained in the elucidation of the central LPS/lipid A recognition and signaling system in mammalian phagocytes. According to the current model, the specific cellular recognition of agonistic LPS/lipid A is initialized by the combined extracellular actions of LPS binding protein (LBP), the membrane-bound or soluble forms of CD14 and the newly identified Toll-like receptor 4 (TLR4)*MD-2 complex, leading to the rapid activation of an intracellular signaling network that is highly homologous to the signaling systems of IL-1 and IL-18. The elucidation of structure-activity correlations in LPS and lipid A has not only contributed to a molecular understanding of both immunostimulatory and toxic septic processes, but has also re-animated the development of new pharmacological and immuno-stimulatory strategies for the prevention and therapy of infectious and malignant diseases.
  • Gene target
    MAb   trachomatis   LPS  
  • Gene symbol
    IRF6
  • Short name
    MAb C. trachomatis LPS
  • Host
    Mouse
  • Isotype
    IgG
  • Alternative name
    monoclonal to C. trachomatis LPS
Gene info
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