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anti-Human IRAK3 Antikörper:
anti-Mouse (Murine) IRAK3 Antikörper:
anti-Rat (Rattus) IRAK3 Antikörper:
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Mouse (Murine) Polyclonal IRAK3 Primary Antibody für ELISA, WB - ABIN409111
Balaci, Spada, Olla, Sole, Loddo, Anedda, Naitza, Zuncheddu, Maschio, Altea, Uda, Pilia, Sanna, Masala, Crisponi, Fattori, Devoto, Doratiotto, Rassu, Mereu, Giua, Cadeddu, Atzeni, Pelosi, Corrias et al.: IRAK-M is involved in the pathogenesis of early-onset persistent asthma. ... in American journal of human genetics 2007
Data indicate a strong positive correlation between interleukin-1 receptor-associated kinase 3 (IRAK-M) and pSTAT3 protein in colorectal cance (zeige STAT3 Antikörper)r (CRC).
IRAK-M functions to modulate inflammatory signaling pathways and is critical in maintaining immune system homeostasis in the gut (zeige GUSB Antikörper). However, increased IRAK-M is associated with increased disease pathogenesis and increased cancer severity in human patients.
Alpha-Melanocyte-Stimulating Hormone (zeige POMC Antikörper) Suppresses TLR2 (zeige TLR2 Antikörper)-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 (zeige HIF1A Antikörper) 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 (zeige TLR7 Antikörper)-induced MEKK3 (zeige MAP3K3 Antikörper)-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 (zeige CBX2 Antikörper) recessive complex 2 repressed the IRAK-M promoter, allowing low levels of expression; following LPS (zeige TLR4 Antikörper) 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 (zeige STAT3 Antikörper) 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 (zeige IL7 Antikörper) reduced IRAK-M expression and attenuated immune tolerance induced by either LPS (zeige TLR4 Antikörper) 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