The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model - Wikidata - awgldk - TriplyDB

The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model

The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model

http://www.wikidata.org/entity/Q24652628

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Novel Roles for Chloride Channels, Exchangers, and Regulators in Chronic Inflammatory Airway Diseases Epithelial Sodium and Chloride Channels and Asthma The cell biology of asthma Novel therapies for the treatment of pertussis disease Barriers to inhaled gene therapy of obstructive lung diseases: A review Do mutations of the Pendred syndrome gene, SLC26A4, confer resistance to asthma and hypertension?Transcriptional regulation of the pendrin gene.Airway surface liquid depth imaged by surface laser reflectance microscopy.Epithelial anion transporter pendrin contributes to inflammatory lung pathology in mouse models of Bordetella pertussis infection Distinct roles of FOXA2 and FOXA3 in allergic airway disease and asthma.IL-17A induces Pendrin expression and chloride-bicarbonate exchange in human bronchial epithelial cells Increased expression of the epithelial anion transporter pendrin/SLC26A4 in nasal polyps of patients with chronic rhinosinusitis Pertussis toxin exacerbates and prolongs airway inflammatory responses during Bordetella pertussis infection.Hypoxia-induced mitogenic factor (HIMF/FIZZ1/RELMα) in chronic hypoxia- and antigen-mediated pulmonary vascular remodeling.The SLC26 gene family of anion transporters and channels.Pendrin, an anion exchanger on lung epithelial cells, could be a novel target for lipopolysaccharide-induced acute lung injury mice.Inhibitors of pendrin anion exchange identified in a small molecule screen increase airway surface liquid volume in cystic fibrosis.Functional characterization of pendrin mutations found in the Israeli and Palestinian populations.Identification of allelic variants of pendrin (SLC26A4) with loss and gain of function.Thiocyanate: a potentially useful therapeutic agent with host defense and antioxidant properties.Pendrin, a novel transcriptional target of the uroguanylin system.Adhesion GPCR Function in Pulmonary Development and Disease.Effects of Allergic Sensitization on Antiviral Immunity: Allergen, Virus, and Host Cell Mechanisms.Interleukin-13 increases pendrin abundance to the cell surface in bronchial NCI-H292 cells via Rho/actin signaling.Exosomes in immunoregulation of chronic lung diseases.STAT6 links IL-4/IL-13 stimulation with pendrin expression in asthma and chronic obstructive pulmonary disease.Thick airway surface liquid volume and weak mucin expression in pendrin-deficient human airway epithelia.Concentration of the antibacterial precursor thiocyanate in cystic fibrosis airway secretions.IL-1β expression in the distal lung epithelium disrupts lung morphogenesis and epithelial cell differentiation in fetal mice.An emerging role of pendrin in health and disease.Small-Molecule Inhibitors of Pendrin Potentiate the Diuretic Action of Furosemide.The Significance of Hypothiocyanite Production via the Pendrin/DUOX/Peroxidase Pathway in the Pathogenesis of Asthma.ATP12A promotes mucus dysfunction during Type 2 airway inflammation.The ESF meeting on "The proteomics, epigenetics and pharmacogenetics of pendrin".Induction of Airway Allergic Inflammation by Hypothiocyanite via Epithelial Cells.Treatment of allergic rhinitis with CpG oligodeoxynucleotides alleviates the lower airway outcomes of combined allergic rhinitis and asthma syndrome via a mechanism that possibly involves in TSLP.Epigen is induced during the interleukin-13-stimulated cell proliferation in murine primary airway epithelial cells.Cerium dioxide nanoparticles exacerbate house dust mite induced type II airway inflammation.Most bicarbonate secretion by Calu-3 cells is mediated by CFTR and independent of pendrin.Potential antiviral activities of camel, bovine, and human lactoperoxidases against hepatitis C virus genotype 4

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P2860

The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model

http://www.wikidata.org/entity/Q24652628

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2008 nî lūn-bûn

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2008 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2008年论文

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The epithelial anion transport ...... nflammation in an asthma model

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The epithelial anion transport ...... nflammation in an asthma model

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The epithelial anion transport ...... nflammation in an asthma model

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The epithelial anion transport ...... nflammation in an asthma model

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The epithelial anion transport ...... nflammation in an asthma model

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The epithelial anion transport ...... nflammation in an asthma model

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JIMMUNOL.181.3.2203

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Journal of Immunology

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The epithelial anion transport ...... nflammation in an asthma model

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P2093

Douglas A Kuperman

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Gregory M Dolganov

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Guohua Zhen

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Homer A Boushey

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Louis T Nguyenvu

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Pedro C Avila

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Silvio Favoreto

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Sung-Woo Park

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Xiaozhu Huang

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Yasuhiro Nakagami

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P2860

The Pendred syndrome gene encodes a chloride-iodide transport protein

Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)

Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion

IL-13 and epidermal growth factor receptor have critical but distinct roles in epithelial cell mucin production

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Pendrin: an apical Cl-/OH-/HCO3- exchanger in the kidney cortex

A calcium-activated chloride channel blocker inhibits goblet cell metaplasia and mucus overproduction

Increased airway epithelial Na+ absorption produces cystic fibrosis-like lung disease in mice

Dissecting asthma using focused transgenic modeling and functional genomics

Identification of pendrin as a common mediator for mucus production in bronchial asthma and chronic obstructive pulmonary disease

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2203-10

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