Human myeloid differentiation factor 88, MyD88 ELISA Kit

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.

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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MYD88 deficiency (MYD88D)

Cytoplasm. Nucleus.

Ubiquitous.

HGNC: 7562

OMIM: 602170

KEGG: hsa:4615

STRING: 9606.ENSP00000401399

UniGene: Hs.82116