Sökning: "CFTR"
Visar resultat 1 - 5 av 29 avhandlingar innehållade ordet CFTR.
1. CFTR in pancreatic islets
Sammanfattning : AbstractCystic fibrosis (CF) is caused by mutations in the anion channel and protein regulator CFTR. The most common co-morbidity in CF is CF-related diabetes (CFRD) affecting ~50% of adult patients. The etiopathology of CFRD is largely unknown but the destruction of the exocrine pancreas is thought to contribute. LÄS MER
2. Advances in Pharmacological Treatment of Cystic Fibrosis
Sammanfattning : Cystic fibrosis (CF) is an inborn, hereditary disease, due to mutations in the gene for a cAMP-activated chloride (Cl-) channel, the cystic fibrosis transmembrane conductance regulator (CFTR). As a result of impaired ion and water transport,the airway mucus is abnormally viscous, which leads to bacterial colonization. LÄS MER
3. Functional Aspects of Epithelia in Cystic Fibrosis and Asthma
Sammanfattning : The cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP activated chloride channel in the apical membrane of epithelial cells, is defective in patients with cystic fibrosis (CF). Research efforts are focused on chloride channel function in order to find a cure for the disease. LÄS MER
4. Towards Pharmacological Treatment of Cystic Fibrosis
Sammanfattning : S-nitrosogluthatione is an endogenous substance, present at decreased levels in the lungs of CF patients and was recently found to induce mature CFTR in airway epithelial CF cell lines. We show that S-nitrosoglutathione in physiological concentrations increases the presence of ΔF508 CFTR in the cell membrane and induces cAMP dependent chloride transport in cystic fibrosis airway epithelial cells. LÄS MER
5. Chloride transport and inflammation in cystic fibrosis airways
Sammanfattning : Cystic fibrosis (CF) is one of the most common lethal, autosomal recessive inherited diseases among Caucasians. It is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel activated by cyclic AMP. LÄS MER