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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
interleukin-1 receptor 1 (show IL1RL1 Proteins)/MyD88 signalling has roles in the development and progression of pulmonary hypertension
Among genotyped patients, nonresponders associated with wild-type MYD88 and mutated CXCR4 (show CXCR4 Proteins) status. Median time to response was 4 weeks
The authors demonstrated that EV71 infection upregulates miR (show MLXIP Proteins)-21, which in turn suppresses EV71-triggered type I IFN production, thus promoting EV71 replication. Furthermore, they demonstrated that miR (show MLXIP Proteins)-21 targets the myeloid differentiation factor 88(MyD88) and interleukin-1 receptor-associated kinase 1(IRAK1 (show IRAK1 Proteins)), which are involved in EV71-induced type I IFN production.
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 (show MUT Proteins)) disease.
our study shows that MYD88 L265P mutation is associated with poor prognosis and high risk of progression in PCNSL patients.
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
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.
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.
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.
The results obtained in the present study demonstrate for the first time that S100A8 (show S100A8 Proteins) as well as MyD88 and NF-B are activated by T3 and that these molecules are directly involved in the thyroid hormone (show PTH Proteins)-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.
Data suggest that histone acetylation drives elevated Stat1 (show STAT1 Proteins)/Myd88 expression in macrophages from mice with type 1 diabetes; this mechanism is exhibited in both peritoneal macrophages and bone marrow-differentiated macrophages. (Stat1 (show STAT1 Proteins) = signal transducer and activator of transcription 1 (show STAT1 Proteins); Myd88 = myeloid differentiation primary response gene 88)
ESAT6 may induce renal injury by promoting miR (show MLXIP Proteins)-155 expression through the TLR-4 (show TLR4 Proteins)/MyD88 signaling pathway in MTB (show NCAPG2 Proteins)-infected mice.
Ultraviolet radiation engages TLR4 (show TLR4 Proteins)/MyD88 as a death signaling complex in macrophages.
Immobilization stress-induced anorexia is mediated independent of MyD88.
TLR4 (show TLR4 Proteins)-MyD88 expression on B1a cells is critical for their IgM (show CD40LG Proteins)-dependent atheroprotection that not only reduced lesion apoptotic cells and necrotic cores, but also decreased CD4 (show CD4 Proteins) and CD8 (show CD8A Proteins) T-cell infiltrates and augmented TGF-beta1 (show TGFB1 Proteins) expression accompanied by reduced lesion inflammatory cytokines TNF-alpha (show TNF Proteins), IL-1beta (show IL1B Proteins), and IL-18 (show IL18 Proteins).
A cell-specific role for MyD88 was determined in the development of chronic ETOH-induced liver injury.
MyD88 signaling in myeloid and dendritic cells is dispensable for IFN-gamma (show IFNG Proteins)-dependent control of type A F. tularensis infection.
Myd88 is a crucial mediator of local and systemic Sjogren's syndrome disease manifestations.
a novel function of MyD88 in the regulation of metabolism that appears to be independent of its known roles in immunity and development.
propose that dMyD88 is the functional homolog of TIRAP (show TIRAP Proteins) and that both proteins function as sorting adaptors to recruit downstream signaling adaptors to activated receptors
DmMyD88 encodes an essential component of the Toll (show TLR4 Proteins) pathway in dorsoventral pattern formation.
We show that there is a direct interaction between Kra and Tube presumably mediated by the death domains present in both proteins.
both the heterodimeric and heterotrimeric complexes form kidney-shaped structures and that Tube is bivalent and has separate high affinity binding sites for dMyD88 and Pelle (show IRAK1 Proteins).
These results suggest that porcine circovirus 2 induces IL-8 (show IL8 Proteins) secretion via the TLR2/MyD88/NF-kappaB (show NFKB1 Proteins) signalling pathway.
At 30 days after autotransplantation of a pig kidney, mRNA expression increases for MyD88.
These results suggest that an MyD88-dependent signaling pathway is present in newborn as well as in adult swine and that it is involved in the innate immune system of these animals.
microbiota-induced, Myd88-dependent signaling inhibits host Notch (show NOTCH1 Proteins) signaling in the intestinal epithelium, thereby promoting secretory cell fate determination
Fish IRF6 (show IRF6 Proteins) is distinguished from the homolog of mammals by being a positive regulator of IFN transcription and phosphorylated by MyD88 and TBK1 (show TBK1 Proteins), suggesting that differences in the IRF6 (show IRF6 Proteins) regulation pattern exist between lower and higher vertebrates.
DrIRF1 works in concert with MyD88 to activate zebrafish IFNvarphi3 but not IFNvarphi1. These results provide insights into the evolving function of IRF1 (show IRF1 Proteins) as a positive IFN regulator.
MyD88 signaling has an important protective role during early pathogenesis.
MyD88-dependent signaling is involved in the innate immune response of the developing zebrafish embryo, a model for the study of vertebrate innate immunity.
L. rhamnosus GR-1 ameliorates the E. coli-induced disruption of cellular ultrastructure, subsequently reducing the percentage of bovine endometrial epithelial cells apoptosis and limiting inflammatory responses, partly via attenuation of MyD88-dependent and MyD88-independent pathway activation
Modulated cytokine expression in Bovine viral diarrhea virus type 2 infected macrophages was associated with decreased MyD88 expression.
The study demonstrates that in cattle, animals heterozygous at the MyD88 A625C polymorphic marker have a 5-fold reduced risk for active pulmonary tuberculosis.
MyD88 plays a functional role in transducing LPS (show IRF6 Proteins) signaling from TLR-4 (show TLR4 Proteins) to downstream effector molecules involved in NF-kappaB (show NFKB1 Proteins) activation
MyD88 interacts with interferon (show IFNA Proteins) regulatory factor (IRF) 3 (show IRF3 Proteins) and IRF7 (show IRF7 Proteins) in Atlantic salmon (Salmo salar)
the salmon MyD88 was cloned and its expression was analysed.
This gene encodes a cytosolic adapter protein that plays a central role in the innate and adaptive immune response. This protein functions as an essential signal transducer in the interleukin-1 and Toll-like receptor signaling pathways. These pathways regulate that activation of numerous proinflammatory genes. The encoded protein consists of an N-terminal death domain and a C-terminal Toll-interleukin1 receptor domain. Patients with defects in this gene have an increased susceptibility to pyogenic bacterial infections. Alternate splicing results in multiple transcript variants.
myeloid differentiation primary response gene (88)
, myeloid differentiation primary response protein MyD88
, myeloid differentiation primary response protein MyD88-B
, Toll/IL-1 receptor binding protein MyD88-B
, myeloid differentiation primary response gene 88
, myeloid differentiation primary response factor 88
, myeloid differentiation factor 88
, myeloid differentiation primary response protein 88
, myeloid differentiation response protein 88