|Tested species reactivity||Human, Mouse|
|Published species reactivity||Human|
|Host / Isotype||Mouse / IgG1|
|Immunogen||Recombinant protein corresponding to amino acids 2 to 160 of human MD-2|
|Purification||Antigen affinity chromatography|
|Contains||0.02% sodium azide|
|Tested Applications||Dilution *|
|Immunocytochemistry (ICC)||20 ug/ml|
|Immunofluorescence (IF)||20 ug/ml|
|Immunohistochemistry (IHC)||2.5 µg/ml|
|Western Blot (WB)||1 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Immunocytochemistry (ICC)||See 1 publications below|
A suggested positive control is MD-2 recombinant protein.
MD-2 is a member of the Toll/interleukin-1 receptor (TIR) family, a group of proteins that include the Toll-like receptors (TLRs). TLRs are signaling molecules that recognize different pathogen-associated molecular patterns (PAMPs) and serve as an important link between the innate and adaptive immune responses. TLR4, the major signaling receptor for lipopolysaccharide (LPS), requires the binding of MD-2 to its extracellular region for maximal response to LPS. The specificity of this response is determined by the species of MD-2; e.g., human MD-2 transfected into mouse cells can cause mouse TLR4 to react to LPS analogs that are normally antagonistic to human but not mouse TLR4.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
MD-2 is involved in the stimulation of matrix metalloproteinase-1 expression by interferon-¿ and high glucose in mononuclear cells - a potential role of MD-2 in Toll-like receptor 4-independent signalling.
MA5-15765 was used in blocking or activating experiment and immunocytochemistry to study the role of MD-2 in the mechanism by which IFN-gamma and high glucose concentrations stimulate mononuclear cell MMP1 expression
|Lu Z,Li Y,Samuvel DJ,Jin J,Zhang X,Lopes-Virella MF,Huang Y||Immunology (140:301)||2013|