A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires' disease - Wikidata - awgldk - TriplyDB

A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires' disease

A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires' disease

http://www.wikidata.org/entity/Q36371497

about

The evolution of vertebrate Toll-like receptors Toll-like receptors and B-cell receptors synergize to induce immunoglobulin class-switch DNA recombination: relevance to microbial antibody responses Pathogen recognition and inflammatory signaling in innate immune defenses Flagellin-deficient Legionella mutants evade caspase-1- and Naip5-mediated macrophage immunity The Tumor Macroenvironment: Cancer-Promoting Networks Beyond Tumor Beds Primary immunodeficiencies of pattern recognition receptors Single nucleotide polymorphisms of Toll-like receptors and susceptibility to infectious diseases Population genetic tools for dissecting innate immunity in humans Toxoplasma gondii- derived profilin triggers human toll-like receptor 5-dependent cytokine production Reptile Toll-like receptor 5 unveils adaptive evolution of bacterial flagellin recognition The role of alveolar epithelial cells in initiating and shaping pulmonary immune responses: communication between innate and adaptive immune systems TLR5 risk-associated haplotype for canine inflammatory bowel disease confers hyper-responsiveness to flagellin Systems biology of innate immunity Incorporation of membrane-anchored flagellin into influenza virus-like particles enhances the breadth of immune responses.MUC1 expression by human airway epithelial cells mediates Pseudomonas aeruginosa adhesion.Identifying recent adaptations in large-scale genomic data Update on Legionnaires' disease: pathogenesis, epidemiology, detection and control.Toll-like receptor 1 polymorphisms affect innate immune responses and outcomes in sepsis.Human leucine-rich repeat proteins: a genome-wide bioinformatic categorization and functional analysis in innate immunity.Toll-like receptor 4 region genetic variants are associated with susceptibility to melioidosis.Full-exon resequencing reveals toll-like receptor variants contribute to human susceptibility to tuberculosis disease.The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes Lemierre's syndrome and genetic polymorphisms: a case report.Mechanisms of Legionella pneumophila-induced interleukin-8 expression in human lung epithelial cells.Nod-like receptors: cytosolic watchdogs for immunity against pathogens.Human TLR1 deficiency is associated with impaired mycobacterial signaling and protection from leprosy reversal reaction.Comparative genomics of Toll-like receptor signalling in five species Toll-like receptor polymorphisms and susceptibility to urinary tract infections in adult women.Pseudomonas aeruginosa LPS or flagellin are sufficient to activate TLR-dependent signaling in murine alveolar macrophages and airway epithelial cells.Genetic variation of the human urinary tract innate immune response and asymptomatic bacteriuria in women.Innate immune recognition of flagellin limits systemic persistence of Brucella The gene history of zebrafish tlr4a and tlr4b is predictive of their divergent functions.A nonsense mutation in TLR5 is associated with survival and reduced IL-10 and TNF-α levels in human melioidosis.Legionella pneumophila evades gamma interferon-mediated growth suppression through interleukin-10 induction in bone marrow-derived macrophages Polymorphisms in the inflammatory pathway genes TLR2, TLR4, TLR9, LY96, NFKBIA, NFKB1, TNFA, TNFRSF1A, IL6R, IL10, IL23R, PTPN22, and PPARG are associated with susceptibility of inflammatory bowel disease in a Danish cohort.Molecular pathogenesis of infections caused by Legionella pneumophila CRP gene variation and risk of community-acquired pneumonia Toll-like receptor 4 polymorphisms are associated with resistance to Legionnaires' disease.Cooperation between multiple microbial pattern recognition systems is important for host protection against the intracellular pathogen Legionella pneumophila.B cell TLRs and induction of immunoglobulin class-switch DNA recombination.

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P2860

A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires' disease

http://www.wikidata.org/entity/Q36371497

description

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A common dominant TLR5 stop co ...... ility to legionnaires' disease

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A common dominant TLR5 stop co ...... ility to legionnaires' disease

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A common dominant TLR5 stop co ...... ility to legionnaires' disease

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A common dominant TLR5 stop co ...... ility to legionnaires' disease

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A common dominant TLR5 stop co ...... ility to legionnaires' disease

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A common dominant TLR5 stop co ...... ility to legionnaires' disease

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A common dominant TLR5 stop co ...... ility to legionnaires' disease

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P2093

Adrian Ozinsky

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Alan Aderem

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Alex Nachman

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Kamilla D Lettinga

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Kelly D Smith

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Lea Schroeder

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Lue Ping Zhao

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Richard J Laws

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Shawn J Skerrett

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Shuying Sue Li

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P2860

TLR4 mutations are associated with endotoxin hyporesponsiveness in humans

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

Toll-like receptors

Innate immune recognition

Consed: a graphical tool for sequence finishing

Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product

Toll-like receptors in the induction of the innate immune response

The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5

Genetics of susceptibility to human infectious disease

Cutting edge: bacterial flagellin activates basolaterally expressed TLR5 to induce epithelial proinflammatory gene expression

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10.1084/JEM.20031220

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10

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Annelies Verbon

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2003-11-01T00:00:00Z

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9003184

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Toll-like receptor

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2194120

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