IRAK2 Antibody #4367
Filter:
- WB
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 62 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
IRAK2 Antibody detects endogeneous levels of total IRAK2 protein. Cross-reactivity was not detected with other family members.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues at the carboxy terminus of mouse IRAK2. Antibodies were purified by protein A and peptide affinity chromatography.
Background
Interleukin-1 (IL-1) receptor-associated kinase (IRAK) is a serine/threonine-specific kinase that can be coprecipitated in an IL-1-inducible manner with the IL-1 receptor (1). The mammalian family of IRAK molecules contains four members (IRAK1, IRAK2, IRAK3/IRAK-M, and IRAK4). The binding of IL-1 to IL-1 receptor type I (IL-1RI) initiates the formation of a complex that includes IL-1RI, AcP, MyD88, and IRAKs (2). IRAK undergoes autophosphorylation shortly after IL-1 stimulation. The subsequent events involve IRAK dissociation from the IL-1RI complex, its ubiquitination, and its association with two membrane-bound proteins: TAB2 and TRAF6. The resulting IRAK-TRAF6-TAB2 complex is then released into the cytoplasm where it activates protein kinase cascades, including TAK1, IKKs, and the stress-activated kinases (3).
Unlike IRAK1 and IRAK4, IRAK2 and IRAK-M do not have significant kinase activity although they can still activate NF-κB when overexpressed (4,5). Antisense oligonucleotide depletion of IRAK2 can inhibit IL-1 mediated NF-κB activation (6).
Unlike IRAK1 and IRAK4, IRAK2 and IRAK-M do not have significant kinase activity although they can still activate NF-κB when overexpressed (4,5). Antisense oligonucleotide depletion of IRAK2 can inhibit IL-1 mediated NF-κB activation (6).
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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