Recombinant Human Myeloid differentiation primary response protein MyD88 (MYD88)

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Code CSB-EP859945HU
Size $224
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  • Based on the SEQUEST from database of E.coli host and target protein, the LC-MS/MS Analysis result of CSB-EP859945HU could indicate that this peptide derived from E.coli-expressed Homo sapiens (Human) MYD88.
  • Based on the SEQUEST from database of E.coli host and target protein, the LC-MS/MS Analysis result of CSB-EP859945HU could indicate that this peptide derived from E.coli-expressed Homo sapiens (Human) MYD88.
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Product Details

Purity
Greater than 85% as determined by SDS-PAGE.
Target Names
MYD88
Uniprot No.
Research Area
Cardiovascular
Alternative Names
Mutant myeloid differentiation primary response 88; MYD 88; Myd88; MYD88_HUMAN; MYD88D; Myeloid differentiation marker 88; Myeloid differentiation primary response 88; Myeloid differentiation primary response gene (88); Myeloid differentiation primary response gene 88; Myeloid differentiation primary response gene; Myeloid differentiation primary response protein MyD88; OTTHUMP00000161718; OTTHUMP00000208595; OTTHUMP00000209058; OTTHUMP00000209059; OTTHUMP00000209060
Species
Homo sapiens (Human)
Source
E.coli
Expression Region
1-296aa
Target Protein Sequence
MAAGGPGAGSAAPVSSTSSLPLAALNMRVRRRLSLFLNVRTQVAADWTALAEEMDFEYLEIRQLETQADPTGRLLDAWQGRPGASVGRLLELLTKLGRDDVLLELGPSIEEDCQKYILKQQQEEAEKPLQVAAVDSSVPRTAELAGITTLDDPLGHMPERFDAFICYCPSDIQFVQEMIRQLEQTNYRLKLCVSDRDVLPGTCVWSIASELIEKRCRRMVVVVSDDYLQSKECDFQTKFALSLSPGAHQKRLIPIKYKAMKKEFPSILRFITVCDYTNPCTKSWFWTRLAKALSLP
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
37.2 kDa
Protein Length
Full Length
Tag Info
N-terminal 6xHis-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.
Troubleshooting and 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.
Description

Introducing our high-quality Recombinant Human MYD88 protein, specifically designed to support your cardiovascular research endeavors. This full-length protein (1-296aa) is expressed in the reputable E.coli expression system, ensuring a reliable and consistent production of a high-purity protein for your experiments. The N-terminal 6xHis-tagged Myeloid differentiation primary response protein MyD88 enables straightforward purification and detection, delivering a trustworthy product for your scientific investigations.

Our Recombinant Human MYD88 protein is characterized by a purity greater than 85% as determined by SDS-PAGE, making it an exceptional choice for your cardiovascular research projects. Available in both liquid and lyophilized powder forms, this meticulously engineered protein is an indispensable tool for understanding the complex mechanisms within the cardiovascular system, providing a solid foundation for your research and driving new discoveries in the field.

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Target Background

Function
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 such as SARS-CoV-2, SARS-CoV and HIV-1, 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.
Gene References into Functions
  1. MYD88(L265P) mutation does not appear to be a determinant of outcome, and its presence may not be a disease-defining feature in Waldenstrom macroglobulinemia. PMID: 29080258
  2. A summary of recent progress on elucidating the molecular and cellular processes affected by the oncogenic L265P mutation of MYD88 (review) . PMID: 30203262
  3. the results of the present study showed significantly higher mRNA expression levels for MYD88 180days post-transplantation in the graft dysfunction group compared to well functioning graft group PMID: 29452169
  4. the expression levels of TLR4/MyD88 were positively correlated with the metastatic potential of breast cancer cells and tumors. The expression levels of TLR4/MyD88 may be used as a biomarker to evaluate the prognosis and guide the treatment of patients with breast cancer. PMID: 30066873
  5. AGAP2-AS1 was upregulated and transcriptionally induced by SP1 in breast cancer..ChIP assays showed that AGAP2-AS1-bound CBP increased the enrichment of H3K27ac at the promoter region of MyD88, thus resulting in the upregulation of MyD88. Gain- and loss-of-function assays confirmed that the NF-kappaB pathway was activated by MyD88 and AGAP2-AS1 PMID: 30157918
  6. Activates the NFkappaB pathway through the Tolllike receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/IkappaBalpha axis. PMID: 29916535
  7. explored the detection method and clinical relevance of MYD88 mutations in Chinese patients with Chronic Lymphocytic Leukemia PMID: 29242635
  8. The combination of Ligusticum chuanxiong and Radix Paeoniae protects against focal cerebral ischaemia via TLR4/MyD88/MAPK/NF-kappaB signalling pathway in rat model of middle cerebral artery stroke. PMID: 29193143
  9. MYD88 Gene Polymorphism is not associated with Chronic Lymphocytic Leukemia. PMID: 29286214
  10. 17.6% of cases with primary CNS diffuse large B-cell lymphoma had homozygous/hemizygous MYD88 mutations, which has not been previously reported PMID: 28856744
  11. MyD88 mutation status did not correlate with overall survival (OS), post-ASCT OS, or progression-free survival (PFS) for Diffuse Large B Cell Lymphoma Patients undergoing Autologous Stem Cell Transplantation. PMID: 28847710
  12. Inducible activation of MyD88 and CD40 in CAR T cells with a small-molecule drug not only enhances their effector function, resulting in potent antitumor activity in preclinical solid tumors, but also enables their remote control post infusion. PMID: 28801306
  13. loss of MyD88 is essential for retinoic acid-facilitated differentiation of human embryonal carcinoma cells. PMID: 28885616
  14. Study supports that MYD88 status is a necessary biomarker in patients with primary cutaneous large B-cell lymphomas for diagnosis, prognosis, and management. PMID: 27189828
  15. Among age >65 patients, the MyD88 L265P mutation portended a worse overall survival compared with the MyD88 wild type PMID: 29258950
  16. Results show that MyD88 protein is necessary to activate autophagy in HSV-1-infected THP-1 cells. PMID: 27509841
  17. confirmed the high prevalence of MYD88 L265P mutation in Waldenstrom macroglobulinaemia patients, as well as in smouldering Waldenstrom macroglobulinaemia; patients with asymptomatic IgM gammopathies carrying the MYD88 L265P mutation showed a trend towards a shorter time to Waldenstrom macroglobulinaemia progression PMID: 27605200
  18. interleukin-1 receptor 1/MyD88 signalling has roles in the development and progression of pulmonary hypertension PMID: 27418552
  19. Results from whole exome sequencing has led to the identification of the MYD88L265P somatic variants in Waldenstrom's Macroglobulinemia, occurring in about 90% of the patients. [review] PMID: 28423722
  20. Among genotyped patients, nonresponders associated with wild-type MYD88 and mutated CXCR4 status. Median time to response was 4 weeks PMID: 27836860
  21. The authors demonstrated that EV71 infection upregulates miR-21, which in turn suppresses EV71-triggered type I IFN production, thus promoting EV71 replication. Furthermore, they demonstrated that miR-21 targets the myeloid differentiation factor 88(MyD88) and interleukin-1 receptor-associated kinase 1(IRAK1), which are involved in EV71-induced type I IFN production. PMID: 28506791
  22. The findings show that among suspected MYD88(WT) WM cases, an alternative clinicopathological diagnosis is common and can impact clinical care. WM patients with MYD88(WT) disease have a high incidence of associated DLBCL events and significantly shorter survival versus those with MYD88(MUT) disease. PMID: 29181840
  23. our study shows that MYD88 L265P mutation is associated with poor prognosis and high risk of progression in PCNSL patients. PMID: 27161435
  24. This study highlights the relative heterogeneity of MYD88-mutant diffuse large B-cell lymphoma (DLBCL), adding to the field's knowledge of the theranostic importance of MYD88 mutations, but also of associated alterations, emphasizing the usefulness of genomic profiling to best stratify patients for targeted therapy PMID: 27923841
  25. mutated MYD88 can be used to identify malignant pleural effusions in WM patients. WM patients with a suspected malignant pleural effusion should be considered for MYD88 mutation testing as part of their workup to establish the aetiology of their pleural effusion. PMID: 27748515
  26. MYD88 L265P mutations, but no other variants, identify a subgroup of diffuse large B-cell lymphoma mainly of activated B-cell like origin, with extranodal involvement and poor outcome. PMID: 26792260
  27. DNA was extracted from CD138+ or CD19+CD138+ sorted cells isolated from the bone marrows of IgM amyloidosis patients. The study reports of MYD88 L265P somatic mutation in IgM-associated light-chain amyloidosis patients. PMID: 27034430
  28. BTK-inhibitor ibrutinib and FK866 resulted in a significant and synergistic anti-Waldenstrom macroglobulinemia cell death, regardless of MYD88 and CXCR4 mutational status. PMID: 27287071
  29. Study found evidence of alterations in the expression of the initial elements of the TLR4 signalling pathway (TLR4, MyD88 and NF-kappaB) in the PFC of patients with schizophrenia. These alterations seem to depend on the presence/absence of antipsychotic treatment at death. Moreover, a polymorphism within the MyD88 gene was significantly associated with schizophrenia risk. PMID: 27070349
  30. The present study demonstrates that MYD-88 L265P mutation may represent the only sensitive marker for the differentiation of CBL-MZ from probable WM. PMID: 27734522
  31. Aqueous fluid from the second patient with intraocular B-cell lymphoma demonstrated a less common mutation in the MYD88 gene associated with B-cell lymphoma. PMID: 29122821
  32. Studies indicate that ibrutinib is active in patients with Waldenstrom macroglobulinemia (WM) and is affected by MYD88 and CXCR4 mutation status. PMID: 28294689
  33. Moreover, anchoring of MyD88 to the cell membrane augments signaling supporting the importance of membrane localization in MyD88-mediated signaling. PMID: 29155181
  34. MyD88 cysteine residues functionally modulate MyD88-dependent NF-kappaB activation, suggesting a link between MyD88 thiol oxidation state and immune signaling. PMID: 27720842
  35. the expression of certain TAM components was reduced as a result of prolonged degradation of MYD88 by Porphyromonas gingivalis infection. PMID: 28076786
  36. MYD88 expression in subcutaneous adipose tissue of obese subjects could be associated with the development of components of Metabolic syndrome. PMID: 28075222
  37. Patients with primary breast and primary female genital tract diffuse large B cell lymphoma have a high frequency of MYD88 mutations. PMID: 28803429
  38. Mutation in the MYD88 gene is associated with lymphoplasmacytic lymphoma and chronic lymphocytic leukemia. PMID: 27840426
  39. the polymorphisms in TLR-MyD88-NF-kappaB signaling pathway confer genetic susceptibility to Type 2 diabetes mellitus and diabetic nephropathy. PMID: 27062898
  40. Here the authors show that MAL TIR domains spontaneously and reversibly form filaments in vitro. They also form cofilaments with TLR4 TIR domains and induce formation of MyD88 assemblies. PMID: 28759049
  41. data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic. PMID: 27869651
  42. Data indicate that 64 patients (57.1%) carried the myeloid differentiation factor 88 protein (MYD88) L265P mutation and 14 patients (12.5%) carried the chemokine (C-X-C motif) receptor 4 (CXCR4) WHIM-like mutation. PMID: 28280994
  43. HCK represents a novel target for therapeutic development in MYD88-mutated Waldenstrom macroglobulinemia and activated-B cell diffuse large B-cell lymphoma, and possibly other diseases driven by mutated MYD88. PMID: 27143257
  44. We found an that enhanced expression of the TLR4-MyD88-NF-kB pathway occurs in GDM placentae, which positively correlates with heightened local IR in placentae and higher maternal hyperglycemia. The TLR4/MyD88/NF-kB pathway may play a potential role in the development of IR in placentae of GDM. PMID: 27340831
  45. We found that over-expression of CRNDE in astrocytes increased the expression of key factors in the toll-like receptor signaling pathway, especially toll-like receptor-3-mediated MyD88-independent pathway.We speculated that CRNDE might trigger inflammation to regulate tumorigenesis and tumor development through the toll-like receptor pathway PMID: 28621230
  46. Data suggest that, in monocytes and macrophages, the interleukin-1B- (IL1B)-stimulated trans-autophosphorylation of IRAK4 (interleukin-1 receptor-associated kinase 4) is initiated by MYD88-induced dimerization of IRAK4. In contrast, IRAK1 (interleukin-1 receptor-associated kinase 1) is inactive in unstimulated monocytes/macrophages and is converted to an active protein kinase in response to IL1B. PMID: 28512203
  47. our data suggest a new role of MyD88 in the development of glucose intolerance and hepatic steatosis. PMID: 27196572
  48. In patient population from Southeast Serbia Myd 88 L265 mutation was not responsible for the development of diffuse large B-cell non Hodgkin lymphoma. PMID: 27837631
  49. FSTL1 displays anti-inflammatory effects against oxidized low-density lipoprotein-induced pro-inflammatory cytokine production via a mechanism that involves the TLR4/MyD88/NF-kappaB and MAPK signaling pathways. PMID: 27569284
  50. The incidence of MYD88 and CD79B mutations in patients with CD5(+) DLBCL is lower than that in patients with DLBCL-SS, suggesting that CD5(+) DLBCL is not the same disease as DLBCL-SS in terms of gene mutation status. PMID: 27915469

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Involvement in disease
MYD88 deficiency (MYD88D)
Subcellular Location
Cytoplasm. Nucleus.
Tissue Specificity
Ubiquitous.
Database Links

HGNC: 7562

OMIM: 602170

KEGG: hsa:4615

STRING: 9606.ENSP00000401399

UniGene: Hs.82116

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