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Data indicate a strong positive correlation between interleukin-1 receptor-associated kinase 3 (IRAK-M) and pSTAT3 protein in colorectal cance (show STAT3 ELISA Kits)r (CRC).
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
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 (show CBX2 ELISA Kits) recessive complex 2 repressed the IRAK-M promoter, allowing low levels of expression; following LPS (show TLR4 ELISA Kits) 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 (show STAT3 ELISA Kits) 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 (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.
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