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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 4

IRAK-4, interleukin-1 receptor-associated kinase 4
This gene encodes a kinase that activates NF-kappaB in both the Toll-like receptor (TLR) and T-cell receptor (TCR) signaling pathways. The protein is essential for most innate immune responses. Mutations in this gene result in IRAK4 deficiency and recurrent invasive pneumococcal disease. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: IRAK, MyD88, IL-1beta, TLR4, CAN
Papers using IRAK-4 antibodies
Interleukin-1 receptor-associated kinase-1 plays an essential role for Toll-like receptor (TLR)7- and TLR9-mediated interferon-α induction
Akira Shizuo et al., In The Journal of Experimental Medicine, 2003
... The cDNA fragments encoding IRAK-1 and IRAK-4 were amplified by PCR from a human spleen cDNA library (CLONTECH Laboratories, Inc.), digested with ...
Papers on IRAK-4
IRAK-4 deficiency as a cause for familial fatal invasive infection by Streptococcus pneumoniae.
Turvey et al., Vancouver, Canada. In Clin Immunol, Jan 2016
UNASSIGNED: In this Letter to the Editor we report the case of two siblings with fatal pneumococcal meningitis as the initial manifestation of IRAK-4 deficiency caused by previously undescribed mutations in IRAK4.
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.
Microarray and whole-exome sequencing analysis of familial Behçet's disease patients.
Nojima et al., Suita, Japan. In Sci Rep, Dec 2015
They include heterozygous SNVs in the genes encoding IL-1 receptor-associated kinase 4 (IRAK4), nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain-containing 14 (NRP14) and melanoma antigen-encoding gene E2 (MAGEE2); IRAK4 harbors a missense mutation, whereas NRP14 and MAGEE2 harbor nonsense mutations.
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
Whereas TLR signaling in mouse macrophages depended primarily on IRAK4 and IRAK2, with little or no role for IRAK1, TLR signaling and proinflammatory cytokine production in human macrophages depended on IRAK1, with knockdown of IRAK4 or IRAK2 having less of an effect.
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.
Role of innate immune system in systemic sclerosis.
O'Reilly et al., Durham, United Kingdom. In Semin Immunopathol, Sep 2015
This has been shown to require both IRAK4 and NF-κB with evidence suggesting autoantibodies bind to RNA to stimulate TIMP-1 production in monocytes.
Interleukin-1 receptor associated kinase inhibitors: potential therapeutic agents for inflammatory- and immune-related disorders.
Silakari et al., Patiāla, India. In Cell Signal, Jun 2015
IRAK-4 has been evaluated as an indispensable element of IL-Rs and TLR pathways that can regulate the abnormal levels of cytokines, and therefore could be employed to manage immune- and inflammation-related disorders.
Recent advances in the discovery of small molecule inhibitors of interleukin-1 receptor-associated kinase 4 (IRAK4) as a therapeutic target for inflammation and oncology disorders.
Romero et al., Cambridge, United States. In J Med Chem, Feb 2015
IRAK4, a serine/threonine kinase, plays a key role in both inflammation and oncology diseases.
Systematic analysis of immunodeficiency.
Tough, Stevenage, United Kingdom. In Nat Immunol, 2014
Humans deficient in the adaptor MyD88 or the kinase IRAK4 suffer from primary immunodeficiency.
A narrow repertoire of transcriptional modules responsive to pyogenic bacteria is impaired in patients carrying loss-of-function mutations in MYD88 or IRAK4.
Chaussabel et al., Dallas, United States. In Nat Immunol, 2014
Loss of function of the kinase IRAK4 or the adaptor MyD88 in humans interrupts a pathway critical for pathogen sensing and ignition of inflammation.
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.
Effect of taurine on IRAK4 and NF-kappa B in Kupffer cells from rat liver grafts after ischemia-reperfusion injury.
Gong et al., Chongqing, China. In Am J Surg, 2012
Data suggest that taurine could protect against hepatic ischemia/reperfusion injury after liver transplantation, and the protective effects may be through downregulation of IRAK-4 in Kupffer cells.
Genetic variation in Toll-like receptors and disease susceptibility.
O'Neill et al., Nijmegen, Netherlands. In Nat Immunol, 2012
First, monogenic disorders associated with complete deficiency in certain TLR pathways, such as MyD88-IRAK4 or TLR3-Unc93b-TRIF-TRAF3, have demonstrated the specific roles of these pathways in host defense against pyogenic bacteria and herpesviruses, respectively.
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.
Induction of endotoxin tolerance in vivo inhibits activation of IRAK4 and increases negative regulators IRAK-M, SHIP-1, and A20.
Medvedev et al., Baltimore, United States. In J Leukoc Biol, 2011
Induction of endotoxin tolerance in vivo inhibits expression of proinflammatory mediators via impaired activation of IRAK4, p38, and NF-kappaB and increases expression of negative regulators of TLR4 pathways.
Interleukin-1 receptor-associated kinase 4 is essential for initial host control of Brucella abortus infection.
Oliveira et al., Belo Horizonte, Brazil. In Infect Immun, 2011
The results shown in this study demonstrated that IRAK-4 is critical to trigger the initial immune response against B. abortus but not at later phases of infection.
Endotoxin tolerance attenuates liver ischemia/reperfusion injury by down-regulation of interleukin-1 receptor-associated kinase 4 in kupffer cells.
Gong et al., Chongqing, China. In Transplant Proc, 2011
expression of IRAK-4 in Kupffer cells may play an important role in the formation of endotoxin tolerance
Oncogenically active MYD88 mutations in human lymphoma.
Staudt et al., Bethesda, United States. In Nature, 2011
RNA interference screening revealed that MYD88 and the associated kinases IRAK1 and IRAK4 are essential for ABC DLBCL survival.
The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88.
Cerutti et al., New York City, United States. In Nat Immunol, 2010
TACI lacks a TIR domain, yet triggered CSR via the DNA-editing enzyme AID by activating NF-kappaB through a Toll-like receptor (TLR)-like MyD88-IRAK1-IRAK4-TRAF6-TAK1 pathway.
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