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IRAK-M functions to modulate inflammatory signaling pathways and is critical in maintaining immune system homeostasis in the gut (show GUSB ELISA Kits). However, increased IRAK-M is associated with increased disease pathogenesis and increased cancer severity in human patients.
Alpha-Melanocyte-Stimulating Hormone (show POMC ELISA Kits) Suppresses TLR2 (show TLR2 ELISA Kits)-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 (show HIF1A ELISA Kits) 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 (show TLR7 ELISA Kits)-induced MEKK3 (show MAP3K3 ELISA Kits)-dependent second wave NFjB activation to produce inhibitory molecules
the tested variations of IRAK-M and SIGIRR (show SIGIRR ELISA Kits) genes do not confer a relevant role in the susceptibility to systemic lupus erythematosus in European-descent populations
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 (show IL7 ELISA Kits) reduced IRAK-M expression and attenuated immune tolerance induced by either LPS (show TLR4 ELISA Kits) 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 (show TYROBP ELISA Kits)/IRAK-M/IL-10 (show IL10 ELISA Kits) to be a novel molecular pathway in APCs (show APCS ELISA Kits) 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 (show TLR4 ELISA Kits) signaling pathway.
Altered gut (show GUSB ELISA Kits) microbiota promotes colitis-associated cancer in IL-1 receptor-associated kinase M-deficient mice.
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