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  4. Recombinant Mouse Myeloid differentiation primary response protein MyD88 (Myd88)

Recombinant Mouse Myeloid differentiation primary response protein MyD88 (Myd88)

  • 货号：
    CSB-YP015282MO
  • 规格：
  • 来源：
    Yeast
  • 其他：
  • 货号：
    CSB-EP015282MO
  • 规格：
  • 来源：
    E.coli
  • 其他：
  • 货号：
    CSB-EP015282MO-B
  • 规格：
  • 来源：
    E.coli
  • 共轭：
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他：
  • 货号：
    CSB-BP015282MO
  • 规格：
  • 来源：
    Baculovirus
  • 其他：
  • 货号：
    CSB-MP015282MO
  • 规格：
  • 来源：
    Mammalian cell
  • 其他：

产品详情

  • 纯度：
    >85% (SDS-PAGE)
  • 基因名：
  • Uniprot No.：
  • 别名：
    Myd88; Myeloid differentiation primary response protein MyD88
  • 种属：
    Mus musculus (Mouse)
  • 蛋白长度：
    Full length protein
  • 表达区域：
    1-296
  • 氨基酸序列
    MSAGDPRVGS GSLDSFMFSI PLVALNVGVR RRLSLFLNPR TPVAADWTLL AEEMGFEYLE IRELETRPDP TRSLLDAWQG RSGASVGRLL ELLALLDRED ILKELKSRIE EDCQKYLGKQ QNQESEKPLQ VARVESSVPQ TKELGGITTL DDPLGQTPEL FDAFICYCPN DIEFVQEMIR QLEQTDYRLK LCVSDRDVLP GTCVWSIASE LIEKRCRRMV VVVSDDYLQS KECDFQTKFA LSLSPGVQQK RLIPIKYKAM KKDFPSILRF ITICDYTNPC TKSWFWTRLA KALSLP
  • 蛋白标签：
    Tag type will be determined during the manufacturing process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 产品提供形式：
    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.
  • 复溶：
    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.
  • 储存条件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期：
    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.
  • 货期：
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事项：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet ：
    Please contact us to get it.

产品评价

靶点详情

  • 功能：
    Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes. Upon TLR8 activation by GU-rich single-stranded RNA (GU-rich RNA) derived from viruses, induces IL1B release through NLRP3 inflammasome activation. MyD88-mediated signaling in intestinal epithelial cells is crucial for maintenance of gut homeostasis and controls the expression of the antimicrobial lectin REG3G in the small intestine. Mediates leukocyte recruitment at the inflammatory site.; Defective in its ability to induce IRAK phosphorylation and NF-kappa-B activation and can function as a negative regulator of activation by IL-1 or lipopolysaccharide (LPS).
  • 基因功能参考文献：
    1. cell-intrinsic and cell-extrinsic MyD88 signaling controls gene expression in conventional dendritic cells and orchestrates immune responses to inhaled allergens PMID: 29067999
    2. Findings confirm that signalling through MyD88 is the primary driver for Lipopolysaccharide-dependent NF-kappaB translocation to the nucleus. The pattern of NF-kappaB dynamics in TRIF-deficient cells does not, however, directly reflect the kinetics of TNFalpha promoter activation, supporting the concept that TRIF-dependent signalling plays an important role in the transcription of this cytokine. PMID: 28469251
    3. Study shows the identification two novel variants of MyD88 gene in mouse. The novel transcript and protein isoform MYD88N1 was expressed in several tissues while the MyD88N2 variant was found only in the brain. The existence of different transcription factors binding sites observed after promoter analysis indicates their role in the critical control of gene expression at different developmental stages. PMID: 29948634
    4. by promoting the initial antigen-specific B cell proliferation and differentiation, B cell-intrinsic MyD88 signaling enhanced both T-independent and T-dependent antibody responses elicited by Bacterial phage Qbeta-derived virus-like particle. This finding will provide additional insight into the role of Toll-Like Receptor signaling in antiviral immunity, autoimmune diseases, and vaccine design. PMID: 29282308
    5. This study demonstrates that the synergistic effect between TLR4 and TLR3 in macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-regulation is dependent on TLR4-MyD88-NF-kappaB signaling. PMID: 28198368
    6. Results provide evidence that Bbsal autophagy prevents autoactivation or enhancement of inflammatory signals by targeting monomeric MyD88. Also, MyD88 was shown to interact with TRAF6. PMID: 28432355
    7. we confirmed the essential role of MyD88-dependent signalling in recruiting neutrophils and controlling P. aeruginosa-induced pulmonary infection PMID: 29450586
    8. MyD88 protein levels are increased during in vitro myogenesis and in conditions that promote skeletal muscle growth in vivo. PMID: 29158520
    9. The results suggested that dioscin prevents LPSinduced ALI through inhibiting the TLR4/MyD88 signaling pathway via upregulation of HSP70. PMID: 29512786
    10. The results indicate that IgM-restricted PCMZL may harbour distinct molecular genetic characteristics, as evidenced by activating MYD88 mutations, which may explain some of the peculiar clinical and histological features found in this population. PMID: 27861728
    11. MyD88 deficiency considerably protected mice from the development of streptozotocin (STZ)-induced diabetes and delayed the onset of diabetes in Non-Obese Diabetic mice. MyD88 signaling in myeloid cells is a critical pathogenic factor in autoimmune diabetes, which is antagonized by TRIF-dependent responses. This depends at least in part on their opposite effects in regulating IDO in phagocytes exposed to apoptotic cells. PMID: 29522531
    12. the present study indicated that MyD88 and TRIF blockades serve notable and equivalent roles in protecting cardiac deterioration from severe sepsis by attenuating cytokine release, reducing neutrophil infiltration and alleviating apoptosis. PMID: 29115392
    13. Results show that interleukin-33 acts to express Schaffer collateral/CA1 long term potentiation (LTP) relevant to spatial learning and memory in a myeloid differentiation factor 88 (MyD88)-dependent manner. PMID: 29147584
    14. We also define the likely cellular candidates for this MyD88-dependent step. These findings suggest that symptom management is possible without ameliorating protective antiviral immune responses PMID: 27435819
    15. The findings suggest that MyD88 in primary sensory neurons plays an active role in regulating IL-1beta signaling and neuroinflammation in the peripheral and the central nervous systems, and contributes to the maintenance of persistent pain. PMID: 27312666
    16. These findings elucidate a novel mechanism of inflammation-associated osteoclastogenesis, which involves TLR4 recognition of gamma-glutamyltranspeptidase and subsequent activation of MyD88-dependent signaling. PMID: 27775020
    17. The intracellular adaptor protein MyD88-independent TLR2 activation induced by Porphyromonas gingivalis stimulates PI3K signaling that drives inflammation but at the same time depresses phagocytosis and enables phagocytosed bacteria to escape lysosomal degradation. PMID: 28848717
    18. Myd88 is regulated by miR-489 in pulmonary fibrosis. PMID: 27506999
    19. The results obtained in the present study demonstrate for the first time that S100A8 as well as MyD88 and NF-B are activated by T3 and that these molecules are directly involved in the thyroid hormone-induced cardiac hypertrophic response. These data suggest that one of the mechanisms underlying T3-dependent cardiac hypertrophy/failure may involve the activation of an inflammatory pathway. PMID: 28161820
    20. Data suggest that histone acetylation drives elevated Stat1/Myd88 expression in macrophages from mice with type 1 diabetes; this mechanism is exhibited in both peritoneal macrophages and bone marrow-differentiated macrophages. (Stat1 = signal transducer and activator of transcription 1; Myd88 = myeloid differentiation primary response gene 88) PMID: 27623388
    21. ESAT6 may induce renal injury by promoting miR-155 expression through the TLR-4/MyD88 signaling pathway in MTB-infected mice. PMID: 28655852
    22. Ultraviolet radiation engages TLR4/MyD88 as a death signaling complex in macrophages. PMID: 27676214
    23. Immobilization stress-induced anorexia is mediated independent of MyD88. PMID: 27391428
    24. TLR4-MyD88 expression on B1a cells is critical for their IgM-dependent atheroprotection that not only reduced lesion apoptotic cells and necrotic cores, but also decreased CD4 and CD8 T-cell infiltrates and augmented TGF-beta1 expression accompanied by reduced lesion inflammatory cytokines TNF-alpha, IL-1beta, and IL-18. PMID: 27930350
    25. A cell-specific role for MyD88 was determined in the development of chronic ETOH-induced liver injury. PMID: 28165624
    26. Myd88 is a crucial mediator of local and systemic Sjogren's syndrome disease manifestations. PMID: 28951424
    27. These results demonstrate that PTX targets the innate immunity through DAP12, FcRgamma, and MyD88 providing new insights into the immunobiology of PTX. PMID: 28089363
    28. the role of the adaptor molecule MyD88 in a mouse model of adenovirus keratitis, is reported. PMID: 27528076
    29. TLR9/MyD88 signaling selectively in CD11c(+) dendritic cells (DCs) strongly enhances murine cytomegalovirus clearance. PMID: 27760315
    30. CD103(-)CD11b(+) dendritic cells instruct both IFNgamma(+) and IL-17(+) T cells, and only the IL-17-inducing antigen presenting cell functions require MyD88. PMID: 27783947
    31. the expression of certain TAM components was reduced as a result of prolonged degradation of MYD88 by Porphyromonas gingivalis infection. PMID: 28076786
    32. Distinct mechanisms downstream of TLR4 signaling mediate myelosuppression and hematopoietic stem cell exhaustion during sepsis through unique effects of MyD88 and TRIF. PMID: 27264973
    33. these data show that both Myd88 and TRIF are necessary for Th17 differentiation in the lungs in response to immunization with lipopolysaccharide PMID: 27328989
    34. this study shows that MyD88-dependent myeloid-derived suppressor cells expansion from donor bone marrow is critical for protection against fatal intestinal graft-vs.-host disease PMID: 26442657
    35. This study reveals that Ehrlichia-induced liver injury and toxic shock are mediated by MyD88-dependent inflammasome activation and autophagy inhibition. PMID: 29049365
    36. These results suggest that S. Typhimurium promotes its systemic growth and dissemination through MyD88 signaling pathways in mesenchymal cells. PMID: 28674182
    37. data are significant in uncovering a latent, but potent, negative-regulatory role for Myd88 and Fcer1g in the late stages of B cell responses; such roles could limit acute responses; however, they could be particularly significant in chronic responses, such as autoimmunity and chronic infection PMID: 28659358
    38. both Myd88(-/-) mouse strains developed some degree of epidermal thickening during the initial stages of IMQ-induced psoriasis, even in the absence of hematopoietic cell activation and infiltration into the skin, suggesting a contribution of MyD88-independent mechanisms in skin-resident stromal cells. PMID: 28642279
    39. The data suggest that MyD88 signaling in dendritic cells (DC) and intestinal epithelial cells (IEC) is both essential and sufficient to induce a full spectrum of host responses upon intestinal infection with Citrobacter rodentium. PMID: 28520792
    40. Downregulation of adaptor protein MyD88 compromises the angiogenic potential of B16 murine melanoma\ PMID: 28662055
    41. data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic. PMID: 27869651
    42. TLR4 agonist MPLA potently induced MyD88-dependent signaling. Neutrophil recruitment after multiple injections of MPLA was reliant on MyD88-dependent signaling. MPLA treatment induced expansion of myeloid progenitors in bone marrow and upregulation of CD11b and shedding of L-selectin by neutrophils, all of which were attenuated in MyD88-deficient mice. PMID: 27354411
    43. Autophagy contributes to macrophage resistance to Leishmania major. Data, including data from studies in knockout mice, suggest a key resistance mechanism involves endosomal signaling via Tlr3/7/9 in macrophages; macrophages deficient for Tlr3/7/9, Unc93b1, or MyD88 fail to undergo L. major-induced autophagy. (TLR = Toll-like receptor; Unc93b1 = unc-93 homolog B1; MyD88 = myeloid differentiation primary response gene 88) PMID: 28607148
    44. MyD88 inhibitor ST2825 attenuates acute cardiac rejection and promotes donor-specific hyporesponsiveness in stringent skin transplant models PMID: 27125343
    45. MyD88 has a divergent requirement for cell survival in non-Tregs and Tregs, and a yet-to-be defined survival-independent requirement for Treg function during the response to alloantigen PMID: 27112509
    46. The aim of this study was to examine the role of the common TLR adaptor protein myeloid-differentiation factor (MyD) 88 in lung epithelium during host defense against K. pneumoniae-induced pneumonia. PMID: 28187270
    47. TLR2, TLR4 AND MyD88 mediate allergic airway disease (AAD) and Streptococcus pneumoniae-induced suppression of AAD. PMID: 27309732
    48. miR-23a-5p modulated the innate host defense by promoting mycobacteria survival and inhibiting the activation of autophagy against Mycobacterium tuberculosis through TLR2/MyD88/NF-kappaB pathway by targeting TLR2. PMID: 28327409
    49. results indicate that the R753Q polymorphism alters TLR2 signaling competence, leading to impaired MyD88-TLR2 assembly, reduced phosphorylation of IRAK-1, diminished activation of MAPKs and NF-kappaB, and deficient induction of cytokines in macrophages infected with M. smegmatis. PMID: 28442574
    50. our data suggest a new role of MyD88 in the development of glucose intolerance and hepatic steatosis. PMID: 27196572

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  • 亚细胞定位：
    Cytoplasm. Nucleus.
  • 组织特异性：
    Detected in bone marrow. Isoform 1 is expressed in testis, kidney, lung, ovary, adrenal gland, provstate, thymus and heart, and weakly in skeletal muscle, liver, spleen and brain. Isoform 2 is mainly expressed in the spleen and weakly in brain.
  • 数据库链接：

    KEGG: mmu:17874

    STRING: 10090.ENSMUSP00000035092

    UniGene: Mm.213003