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Interleukin-1 receptor-associated kinase 3

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. [provided by RefSeq, May 2010] (from NCBI)
Top mentioned proteins: IRAK, TLR4, IL-1beta, TLR2, CAN
Papers using IRAK-M antibodies
Oxidized low-density lipoprotein correlates positively with toll-like receptor 2 and interferon regulatory factor-1 and inversely with superoxide dismutase-1 expression: studies in hypercholesterolemic swine and THP-1 cells.
Mukhopadhyay Partha, In PLoS ONE, 2005
... (D23G12) and TRAF6 (D21G3) were purchased from Cell Signaling Technology (Bioké, Leiden, Netherlands), and polyclonal anti-IRAK3 antibody from Rockland (Tebu-bio, Boechout, Belgium) ...
Product differentiation by analysis of DNA melting curves during the polymerase chain reaction.
Srivastava Rakesh K., In PLoS ONE, 1996
... Polyclonal anti-IRAK3 antibody was purchased from Rockland and Alexa647-conjugated goat anti-rabbit ...
Papers on IRAK-M
Endothelial cell tolerance to lipopolysaccharide challenge is induced by Monophosphoryl lipid A.
Sherwood et al., Nashville, United States. In Clin Sci (lond), Jan 2016
The tolerant phenotype in endothelial cells was associated with reduced IKK, p38 and JNK phosphorylation and enhanced IRAK-M expression for LPS primed HUVECs, but less so in MPLA primed cells.
The role of Interleukin Receptor Associated Kinase (IRAK)-M in regulation of myofibroblast phenotype in vitro, and in an experimental model of non-reperfused myocardial infarction.
Frangogiannis et al., United States. In J Mol Cell Cardiol, Dec 2015
Although IRAK-M is known to suppress inflammatory activation of macrophages, its role in fibroblasts remains unknown.
Vibrio cholerae porin OmpU induces LPS tolerance by attenuating TLR-mediated signaling.
Mukhopadhaya et al., India. In Mol Immunol, Dec 2015
Additionally, OmpU-pretreatment up-regulates expression of IRAK-M, a negative regulator of TLR signaling, in RAW 264.7 mouse macrophage cells upon LPS-stimulation.
MicroRNAs: Regulators of TLR2-Mediated Probiotic Immune Responses.
Mata-Haro et al., Hermosillo, Mexico. In Microrna, Dec 2015
The signaling pathway involved must be tightly regulated in order to be precise and effective; proteins as TNF receptor-associated factor 6 (TRAF6), Interleukin-1 receptor-associated kinase 4 (IRAK4) and Interleukin-1 receptor-associated kinase 3 (IRAK3 or IRAKM) participate in an important way in the nuclear factor kappa B (NF-κB) signaling pathway, which is the main cascade activated in response to probiotics.
Development of Castration Resistant Prostate Cancer Can Be Predicted by a DNA Hypermethylation Profile.
Ropero et al., Getafe, Spain. In J Urol, Dec 2015
Hypermethylation of IRAK3 (HR 13.72), ZNF215 (HR 4.81) and SEPT9 (HR 7.64) were independent markers of prognosis.
Effects of Sequence Variations in Innate Immune Response Genes on Infectious Outcome in Trauma Patients: A Comprehensive Review.
Van Lieshout et al., Rotterdam, Netherlands. In Shock, Nov 2015
The following genes have been studied in populations of trauma patients: CD14, HMGB1, IFNG, IL1A, IL1B, IL1RN, IL4, IL6, IL8, IL10, IL17F, IL18, MBL2, MASP2, FCN2, TLR1, TLR2, TLR4, TLR9, TNF, LTA, GR, MYLK, NLRP3, PRDX6, RAGE, HSPA1B, HSPA1L, HSP90, SERPINE1, IRAK1, IRAK3, VEGFA, LY96, ANGPT2, LBP, MicroRNA, and mtDNA.
Progesterone and the Repression of Myometrial Inflammation: The Roles of MKP-1 and the AP-1 System.
Johnson et al., London, United Kingdom. In Mol Endocrinol, Oct 2015
For example, P4 repression of IL11 and IRAK3 was maintained upon MKP-1 knockdown.
Tolerance and Cross-Tolerance following Toll-Like Receptor (TLR)-4 and -9 Activation Are Mediated by IRAK-M and Modulated by IL-7 in Murine Splenocytes.
Crouser et al., Saint Louis, United States. In Plos One, 2014
MATERIALS AND METHODS: Flt3-expanded splenocytes obtained from wild-type or matching IRAK-M knockout (IRAK-M-/-), C57BL/6, male mice (8-10 weeks old) were treated repeatedly or alternately with either LPS or CpGA DNA, agonists of Toll-like receptor (TLR)-4 and -9, respectively, over successive 24-hour periods.
Comparison of moonlighting guanylate cyclases: roles in signal direction?
Irving et al., Australia. In Biochem Soc Trans, 2014
One example is the interleukin 1 receptor-associated kinase 3 (IRAK3).
The Alpha-Melanocyte-Stimulating Hormone Suppresses TLR2-Mediated Functional Responses through IRAK-M in Normal Human Keratinocytes.
Song et al., Aurora, United States. In Plos One, 2014
To investigate the mechanism of this response in more detail, siRNA of IRAK-M, a negative regulator of TLR signaling, was utilized in these studies.
IL-1 Receptor-Associated Kinase Signaling and Its Role in Inflammation, Cancer Progression, and Therapy Resistance.
Davila et al., Albany, United States. In Front Immunol, 2013
The IRAK family is comprised of four family members, IRAK-1, IRAK-2, IRAK-3 (also known as IRAK-M), and IRAK-4, which play important roles in both positively and negatively regulating the expression of inflammatory molecules.
[Negative regulation of Toll-like receptor signalling].
Choroszyńska et al., Lublin, Poland. In Postepy Hig Med Dosw (online), 2012
They include soluble receptors (sTLR), transmembrane proteins (ST2, SIGIRR, RP105, TRAIL-R) and intracellular inhibitors (SOCS-1, SOCS-3, sMyD88, TOLLIP, IRAK-M, SARM, A20, β-arrestin, CYLD, SHP).
Interleukin 1 receptor-associated kinase m impairs host defense during pneumococcal pneumonia.
van der Poll et al., Amsterdam, Netherlands. In J Infect Dis, 2012
These data suggest that IRAK-M impairs host defense during pneumococcal pneumonia at the primary site of infection at least in part by inhibiting the early immune response.
IRAK-M modulates expression of IL-10 and cell surface markers CD80 and MHC II after bacterial re-stimulation of tolerized dendritic cells.
Kao et al., Ann Arbor, United States. In Immunol Lett, 2012
Along with endotoxin, bacterial sonicate is able to induce refractory tolerance in BM-DCs, and IRAK-M plays a role in modulating cell surface expression of MHC class II and CD80 and release of IL-10 during this tolerance.
IL-13 dampens human airway epithelial innate immunity through induction of IL-1 receptor-associated kinase M.
Chu et al., Denver, United States. In J Allergy Clin Immunol, 2012
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.
IL-1 receptor-associated kinase 3 gene (IRAK3) variants associate with asthma in a replication study in the Spanish population.
Flores et al., In J Allergy Clin Immunol, 2012
The results confirm the importance of the IRAK3 in asthma pathogenesis in the European populations
Interleukin-1 receptor-associated kinase-3 is a key inhibitor of inflammation in obesity and metabolic syndrome.
Holvoet et al., Leuven, Belgium. In Plos One, 2011
Data suggest further evaluation of IRAK3 as a diagnostic and prognostic marker, and as a target for intervention.
The interleukin-1 receptor-associated kinases: critical regulators of innate immune signalling.
Bowie et al., Dublin, Ireland. In Biochem Pharmacol, 2011
The family comprises of four members, IRAK-1, IRAK-2, IRAK-M (IRAK-3) and IRAK-4, and has a role in both positive and negative regulation of signal transduction.
IRAK-M is a negative regulator of Toll-like receptor signaling.
Flavell et al., New Haven, United States. In Cell, 2002
Endotoxin tolerance was significantly reduced in macrophages from IRAK-M knockout mice. IRAK-M regulates TLR signaling and innate immune homeostasis.
Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4.
Yeh et al., Toronto, Canada. In Nature, 2002
12) and IRAK-M.
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