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Page 1
Deficiency in IRAK4 activity attenuates manifestations of murine Lupus.
Murphy M, Pattabiraman G, Manavalan TT, Medvedev AE. Murphy M, et al. Eur J Immunol. 2017 May;47(5):880-891. doi: 10.1002/eji.201646641. Epub 2017 Mar 31. Eur J Immunol. 2017. PMID: 28295231 Free PMC article.
IRAK4 kinase activity is critical for resistance against Streptococcus pneumoniae, but its involvement in autoimmunity is incompletely understood. ...Thus, IRAK4 kinase activity contributes to murine lupus and could represent a new
IRAK4 kinase activity is critical for resistance against Streptococcus pneumoniae, but its involvement in autoimmunity
IRAK4 activity controls immune responses to intracellular bacteria Listeria monocytogenes and Mycobacterium smegmatis.
Pattabiraman G, Murphy M, Agliano F, Karlinsey K, Medvedev AE. Pattabiraman G, et al. J Leukoc Biol. 2018 Oct;104(4):811-820. doi: 10.1002/JLB.2A1117-449R. Epub 2018 May 11. J Leukoc Biol. 2018. PMID: 29749650 Free PMC article.
IL-1 receptor-associated kinase (IRAK) 4 is a central enzyme of the TLR pathways. This study tested the hypothesis that IRAK4 kinase activity is prerequisite for regulating innate immunity during infections with intracellular bacteria. ...Thus, a loss …
IL-1 receptor-associated kinase (IRAK) 4 is a central enzyme of the TLR pathways. This study tested the hypothesis that IRAK4
Induction of endotoxin tolerance in vivo inhibits activation of IRAK4 and increases negative regulators IRAK-M, SHIP-1, and A20.
Xiong Y, Medvedev AE. Xiong Y, et al. J Leukoc Biol. 2011 Dec;90(6):1141-8. doi: 10.1189/jlb.0611273. Epub 2011 Sep 20. J Leukoc Biol. 2011. PMID: 21934070 Free PMC article.
Molecular mechanisms of reprogramming of TLR4 signaling upon in vivo induction of endotoxin tolerance are incompletely understood. We used an in vivo model of endotoxin tolerance, whereby C57BL/6 mice were i.p....Thus, induction of end
Molecular mechanisms of reprogramming of TLR4 signaling upon in vivo induction of endotoxin tolerance are incompletely …
Endotoxin tolerance impairs IL-1 receptor-associated kinase (IRAK) 4 and TGF-beta-activated kinase 1 activation, K63-linked polyubiquitination and assembly of IRAK1, TNF receptor-associated factor 6, and IkappaB kinase gamma and increases A20 expression.
Xiong Y, Qiu F, Piao W, Song C, Wahl LM, Medvedev AE. Xiong Y, et al. J Biol Chem. 2011 Mar 11;286(10):7905-7916. doi: 10.1074/jbc.M110.182873. Epub 2011 Jan 10. J Biol Chem. 2011. PMID: 21220427 Free PMC article.
The impact of endotoxin tolerance on recruitment, post-translational modifications and signalosome assembly of IL-1 receptor-associated kinase (IRAK) 4, IRAK1, TNF receptor-associated factor (TRAF) 6, TGF-beta-activated kinase (TAK) 1, and Ikapp …
The impact of endotoxin tolerance on recruitment, post-translational modifications and signalosome assembly of IL-1 receptor-a …
Cutting edge: expression of IL-1 receptor-associated kinase-4 (IRAK-4) proteins with mutations identified in a patient with recurrent bacterial infections alters normal IRAK-4 interaction with components of the IL-1 receptor complex.
Medvedev AE, Thomas K, Awomoyi A, Kuhns DB, Gallin JI, Li X, Vogel SN. Medvedev AE, et al. J Immunol. 2005 Jun 1;174(11):6587-91. doi: 10.4049/jimmunol.174.11.6587. J Immunol. 2005. PMID: 15905496
In a patient with recurrent bacterial infections and profound hyporesponsiveness to LPS and IL-1, we previously identified two mutations in IL-1R-associated kinase-4 (IRAK-4) that encoded proteins with truncated kinase domains. Overexpression of either of these muta …
In a patient with recurrent bacterial infections and profound hyporesponsiveness to LPS and IL-1, we previously identified two mutations in …
Distinct mutations in IRAK-4 confer hyporesponsiveness to lipopolysaccharide and interleukin-1 in a patient with recurrent bacterial infections.
Medvedev AE, Lentschat A, Kuhns DB, Blanco JC, Salkowski C, Zhang S, Arditi M, Gallin JI, Vogel SN. Medvedev AE, et al. J Exp Med. 2003 Aug 18;198(4):521-31. doi: 10.1084/jem.20030701. J Exp Med. 2003. PMID: 12925671 Free PMC article.
A lack of IL-18 responsiveness, coupled with diminished LPS and/or IL-1-induced nuclear factor-kappaB and activator protein-1 translocation, p38 phosphorylation, gene expression, and dysregulated IL-1R-associated kinase (IRAK)-1 activity in vitro support the …
A lack of IL-18 responsiveness, coupled with diminished LPS and/or IL-1-induced nuclear factor-kappaB and activator protein-1 translo …