Distinct mutations in IRAK-4 confer hyporesponsiveness to lipopolysaccharide and interleukin-1 in a patient with recurrent bacterial infections. - Wikidata - awgldk - TriplyDB

Distinct mutations in IRAK-4 confer hyporesponsiveness to lipopolysaccharide and interleukin-1 in a patient with recurrent bacterial infections.

Distinct mutations in IRAK-4 confer hyporesponsiveness to lipopolysaccharide and interleukin-1 in a patient with recurrent bacterial infections.

http://www.wikidata.org/entity/Q36371624

about

The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88 IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans A TIR domain variant of MyD88 adapter-like (Mal)/TIRAP results in loss of MyD88 binding and reduced TLR2/TLR4 signaling Epidemiology, etiology, pathogenesis, and diagnosis of recurrent bacterial meningitis N. meningitidis and TLR Polymorphisms: A Fascinating Immunomodulatory Network Primary immunodeficiencies of pattern recognition receptors Pathophysiological roles for IL-18 in inflammatory arthritis Selective predisposition to bacterial infections in IRAK-4-deficient children: IRAK-4-dependent TLRs are otherwise redundant in protective immunity NF-kappaB-related genetic diseases The role of interleukin 1 receptor-associated kinase-4 (IRAK-4) kinase activity in IRAK-4-mediated signaling Role of TLR signaling in Francisella tularensis-LPS-induced, antibody-mediated protection against Francisella tularensis challenge.Tolerance induced via TLR2 and TLR4 in human dendritic cells: role of IRAK-1.Synergistic proinflammatory responses induced by polymicrobial colonization of epithelial surfaces Association pattern of interleukin-1 receptor-associated kinase-4 gene polymorphisms with allergic rhinitis in a Han Chinese population.IRAK-4 mutation (Q293X): rapid detection and characterization of defective post-transcriptional TLR/IL-1R responses in human myeloid and non-myeloid cells.Sialyl residues modulate LPS-mediated signaling through the Toll-like receptor 4 complex.Inherited disorders of human Toll-like receptor signaling: immunological implications.Epigenetic contribution to individual variation in response to lipopolysaccharide in bovine dermal fibroblasts.Genetic polymorphisms and posttraumatic complications.Clinical features and outcome of patients with IRAK-4 and MyD88 deficiency.Infectious diseases in patients with IRAK-4, MyD88, NEMO, or IκBα deficiency.A genome-wide association study of variants associated with acquisition of Staphylococcus aureus bacteremia in a healthcare setting.NEMO is a key component of NF-κB- and IRF-3-dependent TLR3-mediated immunity to herpes simplex virus.A nonsynonymous polymorphism of IRAK4 associated with increased prevalence of gram-positive infection and decreased response to toll-like receptor ligands Controlling the Toll road to dendritic cell polarization.Toll-like receptors and the host defense against microbial pathogens: bringing specificity to the innate-immune system.Human genetics of infectious diseases: a unified theory Can innate immunity be enhanced to treat microbial infections?Toll-like receptors in the pathogenesis of human disease.Glucocorticoids: protectors of the brain during innate immune responses.Human disease resulting from gene mutations that interfere with appropriate nuclear factor-kappaB activation.IRAK4 gene polymorphism and odontogenic maxillary sinusitis.Mammalian Toll-like receptors: to immunity and beyond.Alterations in cell signaling in sepsis.Molecular defects in T- and B-cell primary immunodeficiency diseases.Prospects of antiviral and anti-inflammatory therapy for respiratory syncytial virus infection.Impaired innate immunity in mice deficient in interleukin-1 receptor-associated kinase 4 leads to defective type 1 T cell responses, B cell expansion, and enhanced susceptibility to infection with Toxoplasma gondii.The same IkappaBalpha mutation in two related individuals leads to completely different clinical syndromes.Protective and destructive immunity in the periodontium: Part 1--innate and humoral immunity and the periodontium.The role of Toll-like receptors in immune disorders.

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P2860

Distinct mutations in IRAK-4 confer hyporesponsiveness to lipopolysaccharide and interleukin-1 in a patient with recurrent bacterial infections.

http://www.wikidata.org/entity/Q36371624

description

2003 nî lūn-bûn

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2003年の論文

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年學術文章

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2003年學術文章

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2003年學術文章

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name

Distinct mutations in IRAK-4 c ...... ecurrent bacterial infections.

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Distinct mutations in IRAK-4 c ...... ecurrent bacterial infections.

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type

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Distinct mutations in IRAK-4 c ...... ecurrent bacterial infections.

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Distinct mutations in IRAK-4 c ...... ecurrent bacterial infections.

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prefLabel

Distinct mutations in IRAK-4 c ...... ecurrent bacterial infections.

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Distinct mutations in IRAK-4 c ...... ecurrent bacterial infections.

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P1433

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P1433

Journal of Experimental Medicine

P1476

Distinct mutations in IRAK-4 c ...... ecurrent bacterial infections.

@en

P2093

Andrei E Medvedev

http://www.w3.org/2001/XMLSchema#string

Arnd Lentschat

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Cindy Salkowski

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Douglas B Kuhns

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John I Gallin

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Jorge C G Blanco

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Shuling Zhang

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Stefanie N Vogel

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P2860

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

IRAK-4: a novel member of the IRAK family with the properties of an IRAK-kinase

PCR fidelity of pfu DNA polymerase and other thermostable DNA polymerases

IL-1-induced NFkappa B and c-Jun N-terminal kinase (JNK) activation diverge at IL-1 receptor-associated kinase (IRAK)

Impaired cytokine signaling in mice lacking the IL-1 receptor-associated kinase

Pyogenic bacterial infections in humans with IRAK-4 deficiency

Dysregulation of LPS-induced Toll-like receptor 4-MyD88 complex formation and IL-1 receptor-associated kinase 1 activation in endotoxin-tolerant cells

Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4

Cutting edge: functional characterization of the effect of the C3H/HeJ defect in mice that lack an Lpsn gene: in vivo evidence for a dominant negative mutation

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

P304

521-531

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P356

10.1084/JEM.20030701

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P407

P433

4

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P478

198

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10607537

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12925671

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P921

lipopolysaccharide

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2194174

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