Product: SRI-011383 (hydrochloride)
IRAK3 Antibody Summary
| Immunogen |
Peptide with sequence C-GHSYGSKPMEKR corresponding to internal region (near C-Terminus) according to Uniprot Mouse NP_082955.2.
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| Epitope |
GHSYGSKPMEKR
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| Clonality |
Polyclonal
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| Host |
Goat
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| Gene |
IRAK3
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| Purity |
Immunogen affinity purified
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Applications/Dilutions
| Dilutions |
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| Application Notes |
WB: Approx. 65 kDa band observed in rat liver lysates (calculated MW of 67.8 kDa band according to NP_082955.2). An approx. 70 kDa band is observed in mouse bone marrow lysates but this band disappears in lysates from the knock-out mouse.
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| Publications |
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Packaging, Storage & Formulations
| Storage |
Store at -20C. Avoid freeze-thaw cycles.
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| Buffer |
0.5 mg/ml Tris (pH 7.3) and 0.5% BSA
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| Preservative |
0.02% Sodium Azide
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| Concentration |
0.5 mg/ml
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| Purity |
Immunogen affinity purified
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Alternate Names for IRAK3 Antibody
- ASRT5
- EC 2.7.11.1
- FLJ13601
- IL-1 receptor-associated kinase M
- interleukin-1 receptor-associated kinase 3
- IRAK3
- IRAK-3
- IRAKM
- IRAK-M
Background
reduced expression of IRAK-1 and increased expression of IRAK-M after CpG DNA pretreatment resulted in the hyporesponsiveness of macrophages that leads to the protection of mice from hepatic injury and death caused by CpG DNA/D-GalN. Endotoxin tolerance was significantly reduced in macrophages from IRAK-M knockout mice. IRAK-M regulates TLR signaling and innate immune homeostasis. induction of IRAK-M and inhibition of kinase activity of IRAK-1 are crucial to PGN-induced tolerance in macrophages. IRAK-M is a key regulator of the bone loss that is due to osteoclastic resorption of bone. IRAK-M induction negatively regulates Toll-like receptor-dependent interleukin-12 p40 production in macrophages in the presence of Mycobacterium tuberculosis lipoarabinomannan. These findings indicate that IRAK-M selectively attenuates p38 activation and inhibits innate immunity through stabilizing MKP-1. IRAK-M is directly involved in the regulation of both innate and adaptive immune signaling processes, and deletion of IRAK-M enhances host anti-tumor immune response.