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Therefore, the IRAK4-MyD88 scaffolding function is essential for IL-1 signaling, but IRAK4 kinase activity can control IL-1 signal strength by modulating the association of IRAK4, MyD88, and IRAK1.
This article reviews the significance of MYD88(L265P) and CXCR4(WHIM) mutations in the diagnosis and treatment of Waldenstrom Macroglobulinemia [review]
Blocking either STAT3 or IL-10 could significantly increase the susceptibility of MYD88 L265P mutant lymphomas toward CD8(+) T cell-mediated cytotoxicity.
There is an association between increased MyD88 expression and poor survival in high-grade serous ovarian carcinoma; and demonstrates that increased MyD88 expression is also associated with advanced stage high-grade serous ovarian carcinoma.
MYD88 is highly expressed in primary central nervous system lymphoma and is associated with poor survival.
First report of MYD88(L265P) somatic mutation in IgM-associated light chain amyloidosis.
the MYD88 L265P mutation is significantly associated with the tumor sites and molecular subtypes in diffuse large B-cell lymphomas patients (meta-analysis)
Authors reveal the Toll-like receptor (TLR)-associated factor MyD88 as a target of this K63 deubiquitinase activity.
mutational frequencies in CD79B and MYD88 greatly varied with respect to tissue distribution
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.
A summary of recent progress on elucidating the molecular and cellular processes affected by the oncogenic L265P mutation of MYD88 (review) .
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
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.
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
Activates the NFkappaB pathway through the Tolllike receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/IkappaBalpha axis.
explored the detection method and clinical relevance of MYD88 mutations in Chinese patients with Chronic Lymphocytic Leukemia
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.
MYD88 Gene Polymorphism is not associated with Chronic Lymphocytic Leukemia.
17.6% of cases with primary CNS diffuse large B-cell lymphoma had homozygous/hemizygous MYD88 mutations, which has not been previously reported
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.
we found that satellite cell-specific deletion of MyD88 leads to aberrant activation of Notch and Wnt signaling in skeletal muscle of mdx mice. Collectively, our results demonstrate that MyD88-mediated signaling in satellite cells is essential for the regeneration of injured myofibers in dystrophic muscle of mdx mice.
our results indicate that IRAK4 has a critical scaffold function in myddosome formation and that its kinase activity is dispensable for myddosome assembly and activation of the NF-kappaB and MAPK pathways but is essential for MyD88-dependent production of inflammatory cytokines. Our findings suggest that the scaffold function of IRAK4 may be an attractive target for treating inflammatory and autoimmune diseases.
Mice lacking TLR signaling, MyD88-/-, were protected from experimental dry eye-induced ocular surface damage and inflammatory mediator expression, warranting further investigation into TLR inhibition as a potential therapeutic for dry eye disease.
Our findings demonstrate that alkali burn promotes the TLR4-MyD88-caspase-8 axis to cause imbalanced NLRP3/NLRP6, and DS exacerbates ocular surface damage via magnifying this imbalance.
Ablation of inflammsome components reduces SOCS1 induction, and relieves its inhibition on MyD88-IRF7-dependent-IFN-I signaling, leading to high levels of IFN-alpha/beta production and host survival.
Experiments with homozygous knockouts of Irakm (encoding a suppressor of MyD88 inactivation) and Trif in competitive bone marrow transplants revealed that MyD88 is required for High Fat Diet expansion of granulocyte macrophage progenitors and that Trif is required for pregranulocyte macrophage progenitor expansion.
cell-intrinsic and cell-extrinsic MyD88 signaling controls gene expression in conventional dendritic cells and orchestrates immune responses to inhaled allergens
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.
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.
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.
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.
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.
we confirmed the essential role of MyD88-dependent signalling in recruiting neutrophils and controlling P. aeruginosa-induced pulmonary infection
MyD88 protein levels are increased during in vitro myogenesis and in conditions that promote skeletal muscle growth in vivo.
The results suggested that dioscin prevents LPSinduced ALI through inhibiting the TLR4/MyD88 signaling pathway via upregulation of HSP70.
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.
In the initial periods of AP progression, an increased expression of MMP9 in the TLR2 KO and MyD88 KO mice was observed. In the final periods of AP progression, a reduction of MMP2 expression and an increase of MMP9 expression in the TLR2 KO mice were observed. MMP2 and MMP9 production was modulated for TLR2 and MyD88 during apical periodontitis progression
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.
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.
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.
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 and that both proteins function as sorting adaptors to recruit downstream signaling adaptors to activated receptors
DmMyD88 encodes an essential component of the Toll 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.
These results suggest that porcine circovirus 2 induces IL-8 secretion via the TLR2/MyD88/NF-kappaB 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.
suppressed at the mRNA level by intestinal microbial colonization
microbiota-induced, Myd88-dependent signaling inhibits host Notch signaling in the intestinal epithelium, thereby promoting secretory cell fate determination
Fish IRF6 is distinguished from the homolog of mammals by being a positive regulator of IFN transcription and phosphorylated by MyD88 and TBK1, suggesting that differences in the IRF6 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 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 signaling from TLR-4 to downstream effector molecules involved in NF-kappaB activation
MyD88 interacts with interferon regulatory factor (IRF) 3 and IRF7 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