Myeloid differentiation primary response gene 88 is required for the resolution of otitis media - Wikidata - wikimedia - TriplyDB

Myeloid differentiation primary response gene 88 is required for the resolution of otitis media

Myeloid differentiation primary response gene 88 is required for the resolution of otitis media

http://www.wikidata.org/entity/Q36645710

about

Otitis media induced by peptidoglycan-polysaccharide (PGPS) in TLR2-deficient (Tlr2(-/-)) mice for developing drug therapy.Mouse models for human otitis media Increased susceptibility to otitis media in a Splunc1-deficient mouse model Panel 4: Recent advances in otitis media in molecular biology, biochemistry, genetics, and animal models.The toll-Like receptor adaptor TRIF contributes to otitis media pathogenesis and recovery.TNFA deletion alters apoptosis as well as caspase 3 and 4 expression during otitis media.A mouse model of otitis media identifies HB-EGF as a mediator of inflammation-induced mucosal proliferation.HIF-VEGF pathways are critical for chronic otitis media in Junbo and Jeff mouse mutants.CC chemokine ligand 3 overcomes the bacteriocidal and phagocytic defect of macrophages and hastens recovery from experimental otitis media in TNF-/- mice C-Jun N-terminal kinase (JNK) isoforms play differing roles in otitis media Innate signaling in otitis media: pathogenesis and recovery.NOD2/RICK-dependent β-defensin 2 regulation is protective for nontypeable Haemophilus influenzae-induced middle ear infection.The inflammasome adaptor ASC contributes to multiple innate immune processes in the resolution of otitis media.The transcriptome of a complete episode of acute otitis media Innate immunity and the role of defensins in otitis media.Exome sequencing identifies a missense mutation in Isl1 associated with low penetrance otitis media in dearisch mice Peptides actively transported across the tympanic membrane: Functional and structural properties Panel 3: Genetics and Precision Medicine of Otitis Media.Current concepts in the pathogenesis and treatment of chronic suppurative otitis media.Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans Lower nasopharyngeal epithelial cell repair and diminished innate inflammation responses contribute to the onset of acute otitis media in otitis-prone children.Unraveling the genetics of otitis media: from mouse to human and back again.What have we learned from murine models of otitis media?Therapeutic potential of adenovirus-mediated delivery of β-defensin 2 for experimental otitis media.Innate Immunity: Orchestrating Inflammation and Resolution of Otitis Media.Shp2 Deficiency Impairs the Inflammatory Response Against Haemophilus influenzae by Regulating Macrophage Polarization.NOD-Like Receptor Signaling in Cholesteatoma.Otitis Media and Nasopharyngeal Colonization in ccl3-/- Mice.The role of DNA sensing and innate immune receptor TLR9 in otitis media.Both canonical and non-canonical NF-κB activation contribute to the proliferative response of the middle ear mucosa during bacterial infection TLR4-mediated induction of TLR2 signaling is critical in the pathogenesis and resolution of otitis media.Association of microRNA 146 with middle ear hyperplasia in pediatric otitis media.Optimisation of peptides that actively cross the tympanic membrane by random amino acid extension: a phage display study.

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P2860

Myeloid differentiation primary response gene 88 is required for the resolution of otitis media

http://www.wikidata.org/entity/Q36645710

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Myeloid differentiation primar ...... the resolution of otitis media

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Myeloid differentiation primar ...... the resolution of otitis media

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type

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Myeloid differentiation primar ...... the resolution of otitis media

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Myeloid differentiation primar ...... the resolution of otitis media

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Myeloid differentiation primar ...... the resolution of otitis media

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Myeloid differentiation primar ...... the resolution of otitis media

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The Journal of Infectious Diseases

P1476

Myeloid differentiation primar ...... the resolution of otitis media

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P2093

Allen F Ryan

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

Anke Leichtle

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

David H Broide

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Donald G Guiney

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Joerg Ebmeyer

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Kwang Pak

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

Marygorret Obonyo

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

Michelle Hernandez

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

Nicholas J Webster

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Sara Euteneuer

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P2860

Toll-like receptor signalling

Selective predisposition to bacterial infections in IRAK-4-deficient children: IRAK-4-dependent TLRs are otherwise redundant in protective immunity

Identification of Lps2 as a key transducer of MyD88-independent TIR signalling

Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function

Expression of cytokine genes during pneumococcal and nontypeable Haemophilus influenzae acute otitis media in the rat.

Deficiencies of myeloid differentiation factor 88, Toll-like receptor 2 (TLR2), or TLR4 produce specific defects in macrophage cytokine secretion induced by Helicobacter pylori

Mouse models of induced otitis media.

Activation of NF-kappa B by nontypeable Hemophilus influenzae is mediated by toll-like receptor 2-TAK1-dependent NIK-IKK alpha /beta-I kappa B alpha and MKK3/6-p38 MAP kinase signaling pathways in epithelial cells.

Murine macrophages kill the vegetative form of Bacillus anthracis

Morphine induces defects in early response of alveolar macrophages to Streptococcus pneumoniae by modulating TLR9-NF-kappa B signaling.

P304

1862-1869

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scholarly article

P356

10.1086/593213

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P433

12

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198

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2008-12-01T00:00:00Z

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23453479

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18986247

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3584630

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