Product nameIRAK2 peptide
See all IRAK2 proteins and peptides
Our Abpromise guarantee covers the use of ab6233 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Stable for one year.
The pro-inflammatory cytokine IL-1 induces cellular response through two subunits of its receptor, IL-1 receptor I (IL-1RI) and IL-1 receptor accessory protein (IL-1RAcP). IL-1 receptor-associated kinase (IRAK) mediates activation of NF-kB, which is a pivotal transcription factor mediating inflammatory and immune response. A novel member in the IRAK/Pelle family was recently identified and designated IRAK2. Both IRAK and IRAK2 recruit to the subunits of the IL-1R complex after IL-1 binding and lead to NF-kB activation. IRAKs also associate with Toll-like receptor (TLR) and the dominant negative mutants of IRAKs inhibit LPS-induced NF-kB activation. Members in the IRAK/Pelle family play a central role in IL-1R and TLR mediated inflammatory response. IRAK2 is expressed in a variety of human tissues.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Preservative: 0.02% Sodium Azide
Constituents: 0.1% BSA, PBS, pH 7.2
- Interleukin 1 receptor associated kinase 2
- Interleukin 1 receptor associated kinase like 2
FunctionBinds to the IL-1 type I receptor following IL-1 engagement, triggering intracellular signaling cascades leading to transcriptional up-regulation and mRNA stabilization.
Tissue specificityExpressed in spleen, thymus, prostate, lung, liver, skeletal muscle, kidney, pancreas and peripheral blood leukocytes.
Sequence similaritiesBelongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. Pelle subfamily.
Contains 1 death domain.
Contains 1 protein kinase domain.
DomainThe protein kinase domain is predicted to be catalytically inactive.
- Information by UniProt
ab6233 has not yet been referenced specifically in any publications.