|Tested species reactivity||Human, Mouse|
|Published species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide derived from the N-terminal region of the human IRAK4 (IL-1 receptor associated kinase 4) protein.|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS, pH 7.4|
|Contains||0.1% sodium azide|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||3-5 µg/million cells|
|Immunocytochemistry (ICC)||Assay Dependent|
|Immunofluorescence (IF)||Assay Dependent|
|Immunohistochemistry (Paraffin) (IHC (P))||1:10-1:100|
|Western Blot (WB)||Assay Dependent|
* 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.
|Western Blot (WB)||See 1 publications below|
Interleukin-1 (IL-1) and lipopolysaccharide (LPS) induces cellular responses through IL-1 receptor (IL-1R) and Toll-like receptors (TLR). IL-1R-associated kinases (IRAK, IRAK2, and IRAK-M) regulate the activation of NF-kappa-B and MAP kinase (MAPK) by IL-1R/TLR. A novel member in the IRAK/Pelle family was recently identified and designated IRAK-4. Overexpression of IRAK-4 activates NF-kappa-B and MAPK pathways. IRAK-4 interacts with and phosphorylates IRAK-1. IRAK-4-deficient animals are completely resistant to the challenge with LPS. Animals and humans lacking IRAK-4 are impaired in their responses to viral and bacterial challenges. Members in IRAK/Pelle family play a central role in IL-1R/TLR mediated inflammatory responses and in innate immunity.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
|Human||Not Cited||HIV induces both a down-regulation of IRAK-4 that impairs TLR signalling and an up-regulation of the antibiotic peptide dermcidin in monocytic cells.||Pathak S,De Souza GA,Salte T,Wiker HG,Asjö B||Scandinavian journal of immunology (70:264)||2009|