Disease-causing mutations in the cystic fibrosis transmembrane conductance regulator determine the functional responses of alveolar macrophages - Wikidata - awgldk - TriplyDB

Disease-causing mutations in the cystic fibrosis transmembrane conductance regulator determine the functional responses of alveolar macrophages

Disease-causing mutations in the cystic fibrosis transmembrane conductance regulator determine the functional responses of alveolar macrophages

http://www.wikidata.org/entity/Q37467748

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MicroRNA Dysregulation in Cystic Fibrosis TRPC6 channel translocation into phagosomal membrane augments phagosomal function Understanding protein kinase CK2 mis-regulation upon F508del CFTR expression Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner Second-hand cigarette smoke impairs bacterial phagocytosis in macrophages by modulating CFTR dependent lipid-rafts Lysosomal Re-acidification Prevents Lysosphingolipid-Induced Lysosomal Impairment and Cellular Toxicity Presynaptic CLC-3 determines quantal size of inhibitory transmission in the hippocampus 2D luminescence imaging of pH in vivo.The cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in maturation stage ameloblasts, odontoblasts and bone cells Dysfunctional CFTR alters the bactericidal activity of human macrophages against Pseudomonas aeruginosa.Neutrophil-mediated phagocytic host defense defect in myeloid Cftr-inactivated mice.Reactive-oxygen-species-mediated P. aeruginosa killing is functional in human cystic fibrosis macrophages.Abnormal trafficking and degradation of TLR4 underlie the elevated inflammatory response in cystic fibrosis.Pseudomonas aeruginosa-induced bleb-niche formation in epithelial cells is independent of actinomyosin contraction and enhanced by loss of cystic fibrosis transmembrane-conductance regulator osmoregulatory function.Cystic Fibrosis Gene Therapy in the UK and Elsewhere.Toll-like receptor 5 (TLR5), IL-1β secretion, and asparagine endopeptidase are critical factors for alveolar macrophage phagocytosis and bacterial killing.Defective innate immunity and hyperinflammation in newborn cystic fibrosis transmembrane conductance regulator-knockout ferret lungs Activation of Hepatic STAT3 Maintains Pulmonary Defense during Endotoxemia X-Box-Binding Protein 1 and Innate Immune Responses of Human Cystic Fibrosis Alveolar Macrophages.Targeting the Intracellular Environment in Cystic Fibrosis: Restoring Autophagy as a Novel Strategy to Circumvent the CFTR Defect.Intracellular chloride channel protein CLIC1 regulates macrophage function through modulation of phagosomal acidification.Intracellular delivery and trafficking dynamics of a lymphoma-targeting antibody-polymer conjugate.Modulating Innate and Adaptive Immunity by (R)-Roscovitine: Potential Therapeutic Opportunity in Cystic Fibrosis.Low levels of insulin-like growth factor-1 contribute to alveolar macrophage dysfunction in cystic fibrosis.Reduced caveolin-1 promotes hyperinflammation due to abnormal heme oxygenase-1 localization in lipopolysaccharide-challenged macrophages with dysfunctional cystic fibrosis transmembrane conductance regulator.Simultaneous TCR and CD244 signals induce dynamic downmodulation of CD244 on human antiviral T cells.Role of IRE1α/XBP-1 in Cystic Fibrosis Airway Inflammation.Impaired defenses of neonatal mouse alveolar macrophage with cftr deletion are modulated by glutathione and TGFβ1 Cysteamine re-establishes the clearance of Pseudomonas aeruginosa by macrophages bearing the cystic fibrosis-relevant F508del-CFTR mutation.Immune responses in cystic fibrosis: are they intrinsically defective?A review of reagents for fluorescence microscopy of cellular compartments and structures, part I: BacMam labeling and reagents for vesicular structures.Self-assembled hydrogel fibers for sensing the multi-compartment intracellular milieu.Inflammation and its genesis in cystic fibrosis.NAADP/TPC2/Ca(2+) Signaling Inhibits Autophagy.Chloride flux in phagocytes.Staphylococcus aureus Survives in Cystic Fibrosis Macrophages, Forming a Reservoir for Chronic Pneumonia.Inhibition of histone deacetylase 6 improves long-term survival in a lethal septic model.Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH.Lysosomal pH and analysis of the counter ion pathways that support acidification.Optimal complement-mediated phagocytosis of Pseudomonas aeruginosa by monocytes is cystic fibrosis transmembrane conductance regulator-dependent.

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Disease-causing mutations in the cystic fibrosis transmembrane conductance regulator determine the functional responses of alveolar macrophages

http://www.wikidata.org/entity/Q37467748

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bilimsel makale

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scientific article published on December 2009

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vedecký článok

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vetenskaplig artikel

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Disease-causing mutations in t ...... ponses of alveolar macrophages

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Disease-causing mutations in t ...... onses of alveolar macrophages.

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Disease-causing mutations in t ...... ponses of alveolar macrophages

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Disease-causing mutations in t ...... onses of alveolar macrophages.

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Disease-causing mutations in t ...... ponses of alveolar macrophages

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Disease-causing mutations in t ...... onses of alveolar macrophages.

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JBC.M109.057372

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Journal of Biological Chemistry

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Disease-causing mutations in t ...... ponses of alveolar macrophages

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Alexander J Gallan

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

Daniel W Beacham

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

Deborah J Nelson

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Erwin A Gomez

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Guangping Zhang

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

Jessika A Hopson

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Ludmila V Deriy

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Pavel D Shevchenko

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Vytautas P Bindokas

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P2860

Disruption of ClC-3, a chloride channel expressed on synaptic vesicles, leads to a loss of the hippocampus

Anion channels, including ClC-3, are required for normal neutrophil oxidative function, phagocytosis, and transendothelial migration

Co-localization of hydrolytic enzymes with widely disparate pH optima: implications for the regulation of lysosomal pH

Dynamin regulates focal exocytosis in phagocytosing macrophages.

Membrane vesicles as conveyors of immune responses

Lack of acidification in Mycobacterium phagosomes produced by exclusion of the vesicular proton-ATPase

The phagosome: compartment with a license to kill.

Molecular basis for defective glycosylation and Pseudomonas pathogenesis in cystic fibrosis lung.

pH Homeostasis of cellular organelles.

Secretory lysosomes.

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35926-35938

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scholarly article

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10.1074/JBC.M109.057372

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P407

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51

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284

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2009-12-01T00:00:00Z

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19837664

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cystic fibrosis

transmembrane protein

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2791021

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