Recombinant Mouse Interleukin-1 receptor-associated kinase 3(Irak3)

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Code CSB-EP011811MO
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Product Details

Purity Greater than 90% as determined by SDS-PAGE.
Target Names Irak3
Uniprot No. Q8K4B2
Research Area Immunology
Alternative Names Irak3Interleukin-1 receptor-associated kinase 3; IRAK-3; EC; IL-1 receptor-associated kinase M; IRAK-M
Species Mus musculus (Mouse)
Source E.coli
Expression Region 1-609aa
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight 73.5 kDa
Protein Length Full Length
Tag Info N-terminal 10xHis-tagged and C-terminal Myc-tagged
Form Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
and FAQs
Protein FAQs
Storage Condition Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time 3-7 business days
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA Please contact us to get it.

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Target Background

Putative inactive protein kinase which regulates signaling downstream of immune receptors including IL1R and Toll-like receptors. Inhibits dissociation of IRAK1 and IRAK4 from the Toll-like receptor signaling complex by either inhibiting the phosphorylation of IRAK1 and IRAK4 or stabilizing the receptor complex. Upon IL33-induced lung inflammation, positively regulates expression of IL6, CSF3, CXCL2 and CCL5 mRNAs in dendritic cells.
Gene References into Functions
  1. Study using IL-33-induced type 2 immunity signaling in a combination of cell lines, mouse models, and primary cells from mouse models reveal critical roles of IRAK-M and PIN1 in IL-33-induced type 2 immunity. Upon IL-33-induced inflammation, activated PIN1 binds to and catalyzes cis-trans isomerization of phosphorylated IRAK-M, inducing IRAK-M stabilization and nuclear translocation. PMID: 29686383
  2. IRAK3 methylation may be a predictive factor in the transition from colitis to cancer. PMID: 28713897
  3. IRAK-M plays a crucial role in the regulation of allergic airway inflammation by modifying the function of airway epithelia PMID: 28665693
  4. Taken together, these results strongly support a role for IRAK-M in renal injury and identify IRAK-M as a possible modulator in driving an alternatively activated profibrotic macrophage phenotype in unilateral ureteral obstruction-induced chronic kidney disease. PMID: 28701510
  5. polycomb recessive complex 2 repressed the IRAK-M promoter, allowing low levels of expression; following LPS stimulation, the IRAK-M promoter is derepressed, and transcription is induced to allow its expression. PMID: 28011933
  6. this study shows that following Pseudomonas aeruginosa infection, IRAK-M knock-out mice have enhanced lung neutrophilic inflammation and reduced bactertial load PMID: 28120642
  7. Data show that interleukin-1 receptor-associated kinase 3 (IRAK-M) is responsible for regulation of microbial colonization of tumors and STAT3 protein stability in tumor cells, leading to tumor cell proliferation. PMID: 27150039
  8. IRAK-M functions to modulate inflammatory signaling pathways and is critical in maintaining immune system homeostasis in the gut. However, increased IRAK-M is associated with increased disease pathogenesis and increased cancer severity in human patients. PMID: 27939424
  9. IRAK-M may also contribute to myofibroblast conversion. PMID: 26542797
  10. These data demonstrate LTi cells are present in the stomach and promote lymphoid follicle formation in response to infection, but are limited by IRAK-M expression. PMID: 25603827
  11. IL-7 reduced IRAK-M expression and attenuated immune tolerance induced by either LPS or CpGA PMID: 26218271
  12. the results suggest that IRAK-M may be targeted by L. donovani to inhibit TLR-mediated proinflammatory response late during in vitro infection. PMID: 26140693
  13. These data indicate expression of IRAK-M skews lung macrophages toward an alternatively activated profibrotic phenotype, which promotes collagen production, leading to the progression of experimental pulmonary fibrosis. PMID: 25595781
  14. Our study identifies the DAP12/IRAK-M/IL-10 to be a novel molecular pathway in APCs exploited by mycobacterial pathogens, allowing infection a foothold in the lung. PMID: 24172845
  15. This study illustrates how the modulation of innate immune pathways through IRAK-M influences the development of autoimmune diabetes. PMID: 24696448
  16. novel findings provide new insights into the understanding of negative regulatory mechanisms of the TLR4 signaling pathway. PMID: 23872113
  17. Altered gut microbiota promotes colitis-associated cancer in IL-1 receptor-associated kinase M-deficient mice. PMID: 23567778
  18. IRAK-M plays an important role in alcohol-induced liver injury and IRAK-M negatively regulates the innate and possibly the adaptive immune response in the liver reacting to acute insult by alcohol. PMID: 23437317
  19. debris-induced IRAK-M decreases foreign body reactions, but at the same time, the over-expression of IRAK-M may also be detrimental on local intrusion of PAMPs or bacteria PMID: 22941946
  20. IRAK-M mediates TLR7-induced MEKK3-dependent second wave NFjB activation to produce inhibitory molecules PMID: 23376919
  21. IRAK-M impairs host defense during pneumonia caused by a common gram-negative respiratory pathogen. PMID: 22729155
  22. Along with endotoxin, bacterial sonicate is able to induce refractory tolerance in BM-DCs, and IRAK-M plays a role in modulating cell surface expression of MHC class II and CD80 and release of IL-10 during this tolerance. PMID: 22472665
  23. These data suggest that IRAK-M impairs host defense during pneumococcal pneumonia at the primary site of infection at least in part by inhibiting the early immune response. PMID: 22492852
  24. The upregulation of IRAK-M in macrophages is involved in the local immunosuppression around implants, and may contribute to septic and aseptic implant loosening. PMID: 21987497
  25. Endotoxin tolerization in vivo blocked TLR4-driven IRAK4 phosphorylation and activation in macrophages, while increasing expression of IRAK-M, SHIP-1, A20 mRNA, and A20 protein. PMID: 21934070
  26. These data identify a previously unknown function of IRAK-M :suppression of TLR7-mediated autoimmunity-and mutant IRAK-M as a previously unknown genetic risk for murine SLE. PMID: 21875872
  27. Role of IL-1 receptor-associated kinase-M (IRAK-M) in priming of immune and inflammatory responses by nitrogen bisphosphonates. PMID: 21690387
  28. By facilitating IRAK-M expression, DNAX-activation protein (DAP)12 functions to negatively regulate lipopolysaccharide-induced liver dendritic cell maturation. PMID: 21257958
  29. Loss of IRAK-M is associated with colitis. PMID: 20848470
  30. IRAK-M is bound to caspase (CASP)-6 in a complex located near the plasma membrane in resting cells, and the components of this complex redistribute to nucleus and cytoplasm after neutrophil stimulation. PMID: 21098228
  31. findings indicate that systemic sepsis induces epigenetic silencing of cytokine gene expression in lung macrophages, and IRAK-M appears to be a critical mediator of this response PMID: 20585389
  32. manipulation of IRAK-M levels can increase the potency of DC vaccines by enhancing their Ag-presenting function, migration, and longevity PMID: 20817880
  33. these findings suggest that IRAK-M negatively regulates the alternative NFkappaB pathway in a ligand-specific manner. PMID: 19809574
  34. These data suggest that the absence of IRAK-M in the hematopoietic compartment post-bone marrow transplantation enhances pulmonary host defense and mitigates alveolar macrophage sensitivity to the inhibitory effects of PGE(2 PMID: 20439918
  35. IRAK-M is critical to preventing deleterious neutrophil-dependent lung injury during influenza infection of the respiratory tract. PMID: 20042589
  36. Endotoxin tolerance was significantly reduced in macrophages from IRAK-M knockout mice. IRAK-M regulates TLR signaling and innate immune homeostasis. PMID: 12150927
  37. induction of IRAK-M and inhibition of kinase activity of IRAK-1 are crucial to PGN-induced tolerance in macrophages PMID: 14660668
  38. IRAK-M is a key regulator of the bone loss that is due to osteoclastic resorption of bone. PMID: 15809356
  39. IRAK-M induction negatively regulates Toll-like receptor-dependent interleukin-12 p40 production in macrophages in the presence of Mycobacterium tuberculosis lipoarabinomannan PMID: 16263713
  40. These findings indicate that IRAK-M selectively attenuates p38 activation and inhibits innate immunity through stabilizing MKP-1. PMID: 17379480
  41. 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. PMID: 17477969
  42. 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. PMID: 18378686
  43. Tolerance to intraluminally administered LPS in the lymphocyte recruitment process was induced by enterobacteria, possibly via the induction of IRAK-M and TGF-beta. PMID: 19225984
  44. The expression of IRAK-M as a negative regulator of TLR7 signaling was markedly augmented in immune tolerant macrophage-like cells while the interleukin-1 receptor-associated kinase (IRAK)-1 functioned normally. PMID: 19251253
  45. IRAK-M is a major mediator of globular adiponectin-induced endotoxin tolerance in primary macrophages PMID: 19414798
  46. TREM-1 activation beneficially impacts pulmonary IRAK-M expression PMID: 19596984

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Subcellular Location Cytoplasm. Nucleus.
Protein Families Protein kinase superfamily, TKL Ser/Thr protein kinase family, Pelle subfamily
Tissue Specificity Expressed in inflamed lung macrophages (at protein level). Expressed in dendritic cells (at protein level). Highly expressed in liver and thymus and at lower levels in heart, brain, spleen and kidney.
Database Links

KEGG: mmu:73914

STRING: 10090.ENSMUSP00000020448

UniGene: Mm.146194

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