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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Interleukin-1 receptor-associated kinase 1

IRAK, IRAK-1, interleukin-1 receptor-associated kinase, Pelle
This gene encodes the interleukin-1 receptor-associated kinase 1, one of two putative serine/threonine kinases that become associated with the interleukin-1 receptor (IL1R) upon stimulation. This gene is partially responsible for IL1-induced upregulation of the transcription factor NF-kappa B. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: TLR4, MyD88, IL-1beta, IRAK-4, V1a
Papers using IRAK antibodies
MyD88- and Bruton's tyrosine kinase-mediated signals are essential for T cell-independent pathogen-specific IgM responses.
Zimmer Jacques, In PLoS ONE, 2006
... Anti-phosphotyrosine antibody and anti-IRAK-1 antibody was purchased from Cell Signaling Technology (Danvers, MA) ...
Regulation of IL-1 receptor-associated kinases by lipopolysaccharide
Agarwal Sudha, In PLoS ONE, 2001
... against phospho-p38, p38, phospho-JNK, JNK, phospho-ERK 1/2, ERK 1/2, phospho-IKKα/β, IKKβ, phospho-Akt, Akt, phospho-TAK1 and IRAK1 were purchased from Cell Signaling Technology (Danvers, MA, USA) ...
Inhibition of Interleukin 1 Receptor/Toll-like Receptor Signaling through the Alternatively Spliced, Short Form of MyD88 Is Due to Its Failure to Recruit IRAK-4
Tschopp Jürg et al., In The Journal of Experimental Medicine, 1999
... in this study is as follows: anti-Flag/M2 (Eastman Kodak Co.), anti–vesicular stomatitis virus (VSV; Sigma-Aldrich), anti–IRAK-1 (Qbiogene or Santa Cruz Biotechnology, Inc.), anti-MyD88 (ProSci Inc.), ...
Papers on IRAK
Increased Expression of Interleukin-36, a Member of the Interleukin-1 Cytokine Family, in Inflammatory Bowel Disease.
Andoh et al., Ōtsu, Japan. In Inflamm Bowel Dis, Feb 2016
Stimulation with IL-36α and IL-36γ assembled MyD88 adaptor proteins (MyD88, TRAF6, IRAK1, and TAK1) into a complex and induced the activation of NF-κB and AP-1 and also the phosphorylation of MAPKs.
Oxidised LDL induced extracellular trap formation in human neutrophils via TLR-PKC-IRAK-MAPK and NADPH-oxidase activation.
Dikshit et al., Lucknow, India. In Free Radic Biol Med, Feb 2016
UNASSIGNED: Neutrophil extracellular traps (NETs) formation was initially linked with host defence and extracellular killing of pathogens.
MicroRNA-146a Promotes Oligodendrogenesis in Stroke.
Zhang et al., Detroit, United States. In Mol Neurobiol, Feb 2016
MiR-146a also inversely regulated its target gene-IRAK1 expression in OPCs.
Comprehensive RNAi-based screening of human and mouse TLR pathways identifies species-specific preferences in signaling protein use.
Fraser et al., Bethesda, United States. In Sci Signal, Dec 2015
Among these, we identified unexpected differences in the involvement of members of the interleukin-1 receptor-associated kinase (IRAK) family between the human and mouse TLR pathways.
Recurrent Staphylococcus aureus abscess and fatal pneumococcal septicemia due to IRAK-4 deficiency.
Watanabe et al., Tokushima, Japan. In Pediatr Int, Dec 2015
We describe the case of an infant with recurrent episodes of staphylococcal skin abscess and subsequent lethal pneumococcal meningitis/septicemia due to interleukin-1 receptor-associated kinase 4 (IRAK-4) deficiency.
Toll-like receptor signaling in primary immune deficiencies.
Cunningham-Rundles et al., New York City, United States. In Ann N Y Acad Sci, Nov 2015
Defects in interleukin-1 receptor-associated kinase-4 and myeloid differentiation factor 88 (MyD88) lead to susceptibility to infections with bacteria, while mutations in nuclear factor-κB essential modulator (NEMO) and other downstream mediators generally induce broader susceptibility to bacteria, viruses, and fungi.
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.
MicroRNA regulation of viral immunity, latency, and carcinogenesis of selected tumor viruses and HIV.
Ning et al., Johnson City, United States. In Rev Med Virol, Sep 2015
In this review, we summarize the potential roles and mechanisms of viral and cellular miRNAs in the host-pathogen interactions during infection with selected tumor viruses and HIV, which include (i) repressing viral replication and facilitating latency establishment by targeting viral transcripts, (ii) evading innate and adaptive immune responses via toll-like receptors, RIG-I-like receptors, T-cell receptor, and B-cell receptor pathways by targeting signaling molecules such as TRAF6, IRAK1, IKKε, and MyD88, as well as downstream targets including regulatory cytokines such as tumor necrosis factor α, interferon γ, interleukin 10, and transforming growth factor β, (iii) antagonizing intrinsic and extrinsic apoptosis pathways by targeting pro-apoptotic or anti-apoptotic gene transcripts such as the Bcl-2 family and caspase-3, (iv) modulating cell proliferation and survival through regulation of the Wnt, PI3K/Akt, Erk/MAPK, and Jak/STAT signaling pathways, as well as the signaling pathways triggered by viral oncoproteins such as Epstein-Barr Virus LMP1, by targeting Wnt-inhibiting factor 1, SHIP, pTEN, and SOCSs, and (v) regulating cell cycle progression by targeting cell cycle inhibitors such as p21/WAF1 and p27/KIP1.
E3 ubiquitin ligases Pellinos as regulators of pattern recognition receptor signaling and immune responses.
Li et al., Farmington, United States. In Immunol Rev, Jul 2015
Pellinos are a family of E3 ubiquitin ligases discovered for their role in catalyzing K63-linked polyubiquitination of Pelle, an interleukin-1 (IL-1) receptor-associated kinase homolog in the Drosophila Toll pathway.
[Advances in studies on pharmacological action of main chemical constituent of Curcuma Zedoary in preventing in-stent restenosis].
Shi et al., In Zhongguo Zhong Yao Za Zhi, Apr 2015
In recent years, studies have showed that certain extracts and chemical components of E'Zhu could mitigate myocardial cell mitochondria injury and protect vascular endothelium by enhancing heme oxygenase-1 activity, inhibit nuclear factor NF-kappaB, target genes interleukin-associated kinase-1 (IRAK-1), tumor necrosis factor receptor-6 (TRAF-6) and vascular cell adhesion molecule-1 (VCAM-1), reduce inflammatory infiltration, and inhibit growth factor-induced smooth muscle cells (SMCs) proliferation and migration by impacting oxidation of cellular phosphatases.
A cell-intrinsic role for TLR2-MYD88 in intestinal and breast epithelia and oncogenesis.
Clarke et al., Stanford, United States. In Nat Cell Biol, 2014
Inhibition of TLR2, its co-receptor CD14, or its downstream targets MYD88 and IRAK1 inhibits growth of human breast cancers in vitro and in vivo.
The roles of Pellino E3 ubiquitin ligases in immunity.
Moynagh, Ireland. In Nat Rev Immunol, 2014
Pellino proteins were initially characterized as a family of E3 ubiquitin ligases that can catalyse the ubiquitylation of interleukin-1 receptor-associated kinase 1 (IRAK1) and regulate innate immune signalling pathways.
Targeting IRAK1 as a therapeutic approach for myelodysplastic syndrome.
Starczynowski et al., Cincinnati, United States. In Cancer Cell, 2013
We identified that IRAK1, an immune-modulating kinase, is overexpressed and hyperactivated in MDSs.
MYD88 L265P somatic mutation in Waldenström's macroglobulinemia.
Hunter et al., Boston, United States. In N Engl J Med, 2012
This variant predicted an amino acid change (L265P) in MYD88, a mutation that triggers IRAK-mediated NF-κB signaling.
Molecular mechanisms responsible for the selective and low-grade induction of proinflammatory mediators in murine macrophages by lipopolysaccharide.
Li et al., Blacksburg, United States. In J Immunol, 2012
Low-dose lipopolysaccharide utilizes IRAK-1 and Tollip to induce mitochondrial reactive oxygen species, which subsequently induces activating transcription factor (ATF)2 in chronic low-grade inflammatory disease.
Reduced oxidative tissue damage during endotoxemia in IRAK-1 deficient mice.
Li et al., Blacksburg, United States. In Mol Immunol, 2012
we have provided first-hand evidence demonstrating the in vivo beneficial effect of IRAK-1 deficiency in LPS-induced oxidative tissue damage and injury
TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.
Harding et al., Cleveland, United States. In J Immunol, 2012
TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection.
Crh and Oprm1 mediate anxiety-related behavior and social approach in a mouse model of MECP2 duplication syndrome.
Zoghbi et al., Houston, United States. In Nat Genet, 2012
The minimal region shared among affected individuals includes MECP2 and IRAK1, although it is unclear which gene when overexpressed causes anxiety and social behavior deficits.
Identification of interleukin-1 receptor-associated kinase 1 as a critical component that induces post-transcriptional activation of IκB-ζ.
Muta et al., Sendai, Japan. In Febs J, 2012
investigation of signaling components that induce activation of post-transcriptional mechanism for IkappaB-zeta induction/activation: Activation of IRAK1 or IRAK4, but not TRAF6, is sufficient.
Role of IRAK1 on TNF-induced proliferation and NF-ĸB activation in human bone marrow mesenchymal stem cells.
Jung et al., Yangsan, South Korea. In Cell Physiol Biochem, 2011
IRAK1 plays an important role in TNF-alpha-induced nulcear factor kappa B activation in human bone marrow mesenchymal stem cells.
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