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Clinical trial with house dust mite allergen challenge of asthmatic patients reveal that IRAK-M is a PIN1 target critical for IL-33 signaling in allergic asthma. NMR analysis and docking simulations suggest that PIN1 might regulate IRAK-M conformation and function in IL-33 signaling.
Rs11541076 in IRAK3, a negative regulator of TLR signalling, as a predictor of anti-TNF treatment response.
MERS-CoV S protein binds to DPP4 to suppress macrophage activation via induction of IRAK-M, PPARgamma and the immunosuppressive cytokine IL-10.
Data indicate a strong positive correlation between interleukin-1 receptor-associated kinase 3 (IRAK-M) and pSTAT3 protein in colorectal cancer (CRC).
IRAK-M functions to modulate inflammatory signaling pathways and is critical in maintaining immune system homeostasis in the gut. However, increased IRAK-M is associated with increased disease pathogenesis and increased cancer severity in human patients.
Alpha-Melanocyte-Stimulating Hormone Suppresses TLR2-Mediated Functional Responses through IRAK-M in Normal Human Keratinocytes
IRAK3 methylation was associated with tumor stage and poor prognosis of hepatocellular carcinoma patients.
The structure function of the death domain of human IRAK-M
HIF1alpha is a regulator of monocyte functional re-programming in sepsis via regulating IRAKM expression.
IRAK-M expression is upregulated in peripheral blood cells from idiopathic pulmonary fibrosis patients
our study demonstrates that patients carrying IRAK-M+22148 G haplotype are more susceptible to sepsis than patients carrying IRAK-M+22148 A haplotype, suggesting that IRAK-M+22148 G haplotype might be a risk factor for sepsis.
These data indicate the enhancing effect of IRAK-M on epithelial human rhinovirus-16 infection, which is partly through the autophagic pathway.
IRAK-M mediates TLR7-induced MEKK3-dependent second wave NFjB activation to produce inhibitory molecules
the tested variations of IRAK-M and SIGIRR genes do not confer a relevant role in the susceptibility to systemic lupus erythematosus in European-descent populations
these data identify an important signaling regulator in human macrophages that is used by surfactant to control the long-term alveolar inflammatory response, i.e., enhanced IRAK-M activity.
these data indicate that epithelial IRAK-M overexpression in T(H)2 cytokine-exposed airways inhibits TLR2 signaling, providing a novel mechanism for the increased susceptibility of infections in asthmatic patients.
Data suggest further evaluation of IRAK3 as a diagnostic and prognostic marker, and as a target for intervention.
The results confirm the importance of the IRAK3 in asthma pathogenesis in the European populations
The upregulation of IRAK-M in macrophages is involved in the local immunosuppression around implants, and may contribute to septic and aseptic implant loosening.
Common SNPs in the IRAK3 gene may be determinants of sepsis-induced acute lung injury.
Study using IL-33-induced type 2 immunity signaling in a combination of cell lines, mouse models, and primary cells from mouse models reveal critical roles of IRAK-M and PIN1 in IL-33-induced type 2 immunity. Upon IL-33-induced inflammation, activated PIN1 binds to and catalyzes cis-trans isomerization of phosphorylated IRAK-M, inducing IRAK-M stabilization and nuclear translocation.
IRAK3 methylation may be a predictive factor in the transition from colitis to cancer.
IRAK-M plays a crucial role in the regulation of allergic airway inflammation by modifying the function of airway epithelia
Taken together, these results strongly support a role for IRAK-M in renal injury and identify IRAK-M as a possible modulator in driving an alternatively activated profibrotic macrophage phenotype in unilateral ureteral obstruction-induced chronic kidney disease.
polycomb recessive complex 2 repressed the IRAK-M promoter, allowing low levels of expression; following LPS stimulation, the IRAK-M promoter is derepressed, and transcription is induced to allow its expression.
this study shows that following Pseudomonas aeruginosa infection, IRAK-M knock-out mice have enhanced lung neutrophilic inflammation and reduced bactertial load
Data show that interleukin-1 receptor-associated kinase 3 (IRAK-M) is responsible for regulation of microbial colonization of tumors and STAT3 protein stability in tumor cells, leading to tumor cell proliferation.
IRAK-M may also contribute to myofibroblast conversion.
These data demonstrate LTi cells are present in the stomach and promote lymphoid follicle formation in response to infection, but are limited by IRAK-M expression.
IL-7 reduced IRAK-M expression and attenuated immune tolerance induced by either LPS or CpGA
the results suggest that IRAK-M may be targeted by L. donovani to inhibit TLR-mediated proinflammatory response late during in vitro infection.
These data indicate expression of IRAK-M skews lung macrophages toward an alternatively activated profibrotic phenotype, which promotes collagen production, leading to the progression of experimental pulmonary fibrosis.
Our study identifies the DAP12/IRAK-M/IL-10 to be a novel molecular pathway in APCs exploited by mycobacterial pathogens, allowing infection a foothold in the lung.
This study illustrates how the modulation of innate immune pathways through IRAK-M influences the development of autoimmune diabetes.
novel findings provide new insights into the understanding of negative regulatory mechanisms of the TLR4 signaling pathway.
Altered gut microbiota promotes colitis-associated cancer in IL-1 receptor-associated kinase M-deficient mice.
IRAK-M plays an important role in alcohol-induced liver injury and IRAK-M negatively regulates the innate and possibly the adaptive immune response in the liver reacting to acute insult by alcohol.
debris-induced IRAK-M decreases foreign body reactions, but at the same time, the over-expression of IRAK-M may also be detrimental on local intrusion of PAMPs or bacteria
This gene encodes a member of the interleukin-1 receptor-associated kinase protein family. Members of this family are essential components of the Toll/IL-R immune signal transduction pathways. This protein is primarily expressed in monocytes and macrophages and functions as a negative regulator of Toll-like receptor signaling. Mutations in this gene are associated with a susceptibility to asthma. Alternate splicing results in multiple transcript variants.
interleukin-1 receptor-associated kinase 3
, interleukin-1 receptor-associated kinase 3-like
, IL-1 receptor-associated kinase M
, interleukin-1 receptor-associated kinase M