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Molecular Chaperones as Targets to Circumvent the CFTR Defect in Cystic FibrosisThe Concise Guide to PHARMACOLOGY 2013/14: ion channelsMarked increases in mucociliary clearance produced by synergistic secretory agonists or inhibition of the epithelial sodium channel.Calcium-calmodulin does not alter the anion permeability of the mouse TMEM16A calcium-activated chloride channel.International Union of Basic and Clinical Pharmacology. LXXXV: calcium-activated chloride channels.Novel small molecule epithelial sodium channel inhibitors as potential therapeutics in cystic fibrosis - a patent evaluation.Low temperature and chemical rescue affect molecular proximity of DeltaF508-cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial sodium channel (ENaC)Suppression of premature termination codons as a therapeutic approach.Local modulation of cystic fibrosis conductance regulator: cytoskeleton and compartmentalized cAMP signalling.Reduced Arylsulfatase B activity in leukocytes from cystic fibrosis patientsCFTR: folding, misfolding and correcting the ΔF508 conformational defect.Ca2+-activated Cl- channels at a glance.The challenges and promises of new therapies for cystic fibrosis.The cystic fibrosis of exocrine pancreasImpact of salt exposure on N-acetylgalactosamine-4-sulfatase (arylsulfatase B) activity, glycosaminoglycans, kininogen, and bradykinin.Cystic fibrosis transmembrane conductance regulator-mRNA delivery: a novel alternative for cystic fibrosis gene therapy.Molecular, biophysical, and pharmacological properties of calcium-activated chloride channels.Purinergic regulation of CFTR and Ca(2+)-activated Cl(-) channels and K(+) channels in human pancreatic duct epithelium.Asymmetric 4-aryl-1,4-dihydropyridines potentiate mutant cystic fibrosis transmembrane conductance regulator (CFTR).CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer.Pseudohalide anions reveal a novel extracellular site for potentiators to increase CFTR function.Mutations of Cystic Fibrosis Transmembrane Conductance Regulator Gene Cause a Monocyte-Selective Adhesion Deficiency.Hematopoietic stem/progenitor cells express functional mitochondrial energy-dependent cystic fibrosis transmembrane conductance regulator.Increased apical Na+ permeability in cystic fibrosis is supported by a quantitative model of epithelial ion transport.Special issue of BJP on respiratory pharmacology.Innovations in the treatment of cystic fibrosis: outriders for the treatment of diseases with other genetic defects?
P2860
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P2860
description
2011 nî lūn-bûn
@nan
2011 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
New horizons in the treatment of cystic fibrosis.
@ast
New horizons in the treatment of cystic fibrosis.
@en
type
label
New horizons in the treatment of cystic fibrosis.
@ast
New horizons in the treatment of cystic fibrosis.
@en
prefLabel
New horizons in the treatment of cystic fibrosis.
@ast
New horizons in the treatment of cystic fibrosis.
@en
P2860
P1476
New horizons in the treatment of cystic fibrosis.
@en
P2093
A W Cuthbert
P2860
P304
P356
10.1111/J.1476-5381.2010.01137.X
P407
P577
2011-05-01T00:00:00Z