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  4. Recombinant Mouse Interleukin-1 receptor-associated kinase 4 (Irak4)

Recombinant Mouse Interleukin-1 receptor-associated kinase 4 (Irak4)

  • 中文名稱：
    小鼠Irak4重組蛋白
  • 貨號：
    CSB-EP011812MOa0
  • 規格：
    ￥1536
  • 圖片：
    • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
  • 其他：

產品詳情

  • 純度：
    Greater than 90% as determined by SDS-PAGE.
  • 生物活性：
    Not Test
  • 基因名：
  • Uniprot No.：
  • 別名：
    IRAK-4
  • 種屬：
    Mus musculus (Mouse)
  • 蛋白長度：
    Full Length
  • 來源：
    E.coli
  • 分子量：
    57.8
  • 表達區域：
    1-459aa
  • 氨基酸序列
    MNKPLTPSTYIRNLNVGILRKLSDFIDPQEGWKKLAVAIKKPSGDDRYNQFHIRRFEALLQTGKSPTCELLFDWGTTNCTVGDLVDLLVQIELFAPATLLLPDAVPQTVKSLPPREAATVAQTHGPCQEKDRTSVMPMPKLEHSCEPPDSSSPDNRSVESSDTRFHSFSFHELKSITNNFDEQPASAGGNRMGEGGFGVVYKGCVNNTIVAVKKLGAMVEISTEELKQQFDQEIKVMATCQHENLVELLGFSSDSDNLCLVYAYMPNGSLLDRLSCLDGTPPLSWHTRCKVAQGTANGIRFLHENHHIHRDIKSANILLDKDFTAKISDFGLARASARLAQTVMTSRIVGTTAYMAPEALRGEITPKSDIYSFGVVLLELITGLAAVDENREPQLLLDIKEEIEDEEKTIEDYTDEKMSDADPASVEAMYSAASQCLHEKKNRRPDIAKVQQLLQEMSA
    Note: The complete sequence may include tag sequence, target protein sequence, linker sequence and extra sequence that is translated with the protein sequence for the purpose(s) of secretion, stability, solubility, etc.
    If the exact amino acid sequence of this recombinant protein is critical to your application, please explicitly request the full and complete sequence of this protein before ordering.
  • 蛋白標簽：
    N-terminal 6xHis-tagged
  • 產品提供形式：
    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.
  • 緩沖液：
    If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose.
  • 復溶：
    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℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 儲存條件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保質期：
    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.
  • 貨期：
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
  • 注意事項：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4℃ for up to one week.
  • Datasheet & COA：
    Please contact us to get it.

產品評價

靶點詳情

  • 功能：
    Serine/threonine-protein kinase that plays a critical role in initiating innate immune response against foreign pathogens. Involved in Toll-like receptor (TLR) and IL-1R signaling pathways. Is rapidly recruited by MYD88 to the receptor-signaling complex upon TLR activation to form the Myddosome together with IRAK2. Phosphorylates initially IRAK1, thus stimulating the kinase activity and intensive autophosphorylation of IRAK1. Phosphorylates E3 ubiquitin ligases Pellino proteins (PELI1, PELI2 and PELI3) to promote pellino-mediated polyubiquitination of IRAK1. Then, the ubiquitin-binding domain of IKBKG/NEMO binds to polyubiquitinated IRAK1 bringing together the IRAK1-MAP3K7/TAK1-TRAF6 complex and the NEMO-IKKA-IKKB complex. In turn, MAP3K7/TAK1 activates IKKs (CHUK/IKKA and IKBKB/IKKB) leading to NF-kappa-B nuclear translocation and activation. Alternatively, phosphorylates TIRAP to promote its ubiquitination and subsequent degradation. Phosphorylates NCF1 and regulates NADPH oxidase activation after LPS stimulation suggesting a similar mechanism during microbial infections.
  • 基因功能參考文獻：
    1. data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic. PMID: 27869651
    2. IRAK4 kinase activity contributes to murine lupus and could represent a new therapeutic target. PMID: 28295231
    3. Data demonstrate that IRAK-4 is essential for innate and adaptive immunity and necessary for efficient control of mycobacterial infections. PMID: 27439514
    4. Suppression of IRAK1 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding-Defective Mutant of ABIN1 PMID: 27807192
    5. PMA treatment during a vulnerable period can alter brain development. IL-18 and IRAK-4 appear to be important for the development of PMA induced injury. PMID: 25918710
    6. enforced expression of miR-302b or IRAK4 siRNA silencing inhibits downstream NF-kappaB signalling and airway leukocyte infiltration, thereby alleviating lung injury and increasing survival in P. aeruginosa-infected mice. PMID: 24717937
    7. Our results demonstrate that osteoclasts and FBGCs are reciprocally regulated and identify IRAK4 as a potential therapeutic target to inhibit stimulated osteoclastogenesis and rescue inhibited FBGC formation PMID: 25404736
    8. Suggest FC-99 is a potential therapeutic molecule that alleviated experimental sepsis by directly inhibiting IRAK4 activation. PMID: 24588661
    9. MiR-93 inhibits IRAK4 expression by binding directly to the 3'-UTR of IRAK4. PMID: 24642374
    10. Intact IRAK4 function inhibited heart-specific migration of bone-marrow-derived CCR5(+) cells. PMID: 24030499
    11. In macrophages from IRAK4(KDKI) mice, IRAK4 kinase deficiency decreased LPS signaling but did not prevent endotoxin tolerance. A TLR2-TLR1 agonist attenuated TLR2-elicited homo- & heterotolerance at the level of MAPK activation. PMID: 23695305
    12. During bacterial infection, PGN-mediated TLR2 signaling induces miR-132/-212 to downregulate IRAK4. PMID: 23264652
    13. IRAK4-deficient mice exhibit increased susceptibility and decreased cytokine production in vivo upon Streptococcus pneumoniae infection. PMID: 23209321
    14. Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans. PMID: 23255009
    15. Signaling via IRAK4 is essential for the activation of innate immune cells, development of parasite-specific acquired immunity, and host resistance to infection with T. gondii. PMID: 23027530
    16. Induction of endotoxin tolerance in vivo inhibits expression of proinflammatory mediators via impaired activation of IRAK4, p38, and NF-kappaB and increases expression of negative regulators of TLR4 pathways. PMID: 21934070
    17. The results shown in this study demonstrated that IRAK-4 is critical to trigger the initial immune response against B. abortus but not at later phases of infection. PMID: 21844234
    18. Functional deficiency of IRAK4 kinase activity is required for modified low-density lipoprotein-induced NF-kappaB activation and expression of a subset of proinflammatory genes and development of atherosclerosis. PMID: 21278342
    19. Although IRAK4 kinase activity is essential for human plasmacytoid dendritic cell activation, it is dispensable in B, T, dendritic, and monocytic cells, which is in contrast with an essential active kinase role in comparable mouse cell types. PMID: 21160042
    20. This study investigates the potential role of the Toll-like receptor 4 pathway, in particular IRAK-4, in a murine model of acute pancreatitis. PMID: 19434478
    21. MyD88s acts as a negative regulator of IL-1R/TLR/MyD88-triggered signals, leading to a transcriptionally controlled negative regulation of innate immune responses. PMID: 12538665
    22. Irak4 is required for the majority of IL-18-mediated functions both in vitro and in vivo; Th1 cells lacking Irak4 fail to produce IFN-gamma and undergo proliferation in response to IL-18. PMID: 12682231
    23. IRAK-4 is required for induction of IP-10 and IFN-beta, for efficient dendritic cell (DC) maturation, and for lipopolysaccharide-induced cytokine secretion and T helper cell instruction by DCs. PMID: 14634120
    24. IRAK-4 is an integral part of the IL-1R signaling cascade and is capable of transmitting signals both dependent on and independent of its kinase activity PMID: 15292196
    25. Analysis of the crystal structure for the death domain of Mus musculus IRAK-4 reveals a six-helical bundle with a highly structured loop, unique to IRAK-4. PMID: 16177054
    26. findings suggest that T cells use IRAK-4, a critical regulator of innate immunity for the development of acquired immunity, suggesting that IRAK-4 may be involved in direct signal cross talk between the two systems PMID: 16574867
    27. IRAK4, but not IRF3, controls C. pneumoniae-induced IFN-alpha and IFN-gamma secretion and bacterial growth. IRAK4 and IRF3 are redundant for infection-induced NF-kappaB activation, which is regulated by TRAF6. PMID: 17360955
    28. IRAK4 kinase activity plays a critical role in TLR-dependent immune responses. PMID: 17470642
    29. IRAK-4 protein and its kinase activity plays an essential role in Toll-like receptor-mediated immune responses but not in TCR signaling. PMID: 17485511
    30. ST2825 interfered with recruitment of IRAK1 and IRAK4 by MyD88, causing inhibition of IL-1beta-mediated activation of NF-kappaB transcriptional activity. PMID: 17548806
    31. IRAK4 kinase-inactive knock-in ApoE-/- knockout mice were resistant to atherogenesis which further unravels mechanisms of vascular inflammation and identifies IRAK4 as a potential therapeutic target. PMID: 18190779
    32. In IRAK-4 kinase inactive transgenic mice certain LPS signaling pathways and certain aspect of macrophage activation are affected, while others remain unaffected. IRAK-4 kinase activity seems to be important for a more sustained anti-bacterial response. PMID: 18266302
    33. Results indicate that IRAK-4 kinase activity is required for IRAK-4-dependent signaling in innate and adaptive immunity. PMID: 18286567
    34. IRAK-4 kinase activity plays a critical role in IL-1R-, TLR4-, and TLR7-mediated induction of inflammatory responses PMID: 18510099
    35. Interleukin-1 receptor-associated kinase -4 in Toll-Like Receptors signalling pathways; tolerance coincided with IRAK-4 down-regulation which occurred at the protein level via proteolytic degradation as well as at the mRNA level. PMID: 18992325
    36. IRAK-4 is a key component for the development of proarthritis inflammation, but that it is not crucial for T cell activation. PMID: 19479877
    37. Absence of IRAK4 kinase activity leads to delayed onset of autoimmune encephalomyelitis with reduced mononuclear cell infiltration of the spinal cord and a lack of CD4-positive T helper (Th) cell-mediated interleukin (IL)-17 production. PMID: 19542468
    38. Deletion of IRAK-4 has favorable effects on survival and left ventricular remodeling after myocardial infarct by modifying the host inflammatory process. PMID: 19770394

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  • 亞細胞定位：
    Cytoplasm.
  • 蛋白家族：
    Protein kinase superfamily, TKL Ser/Thr protein kinase family, Pelle subfamily
  • 數據庫鏈接：


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