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Regulation of CFTR Endocytosis by the Vasoactive Intestinal Peptide: Role of PKCε

dc.contributor.authorAlshafie, Walaa
dc.contributor.copyright-releaseNot Applicableen_US
dc.contributor.degreeMaster of Scienceen_US
dc.contributor.departmentDepartment of Physiology & Biophysicsen_US
dc.contributor.ethics-approvalNot Applicableen_US
dc.contributor.external-examinerDr. Ryan Pelisen_US
dc.contributor.graduate-coordinatorDr. Robert Roseen_US
dc.contributor.manuscriptsNot Applicableen_US
dc.contributor.thesis-readerDr. Younes Anini, Dr. Xianping Dongen_US
dc.contributor.thesis-supervisorDr Valerie Chappeen_US
dc.date.accessioned2013-12-10T18:40:34Z
dc.date.available2013-12-10T18:40:34Z
dc.date.defence2013-12-02
dc.date.issued2013-12-10
dc.description.abstractThe Vasoactive Intestinal Peptide (VIP) is an agonist of the CFTR chloride channel in the human airways. In the genetic disease Cystic Fibrosis, where CFTR is defective or absent from the apical membrane of epithelial cells, VIP innervations are lost. Our group has demonstrated that VIP increases CFTR membrane stability through PKCε. However, the mechanism remained to be determined. Here we found that VIP stimulation increases the interaction of NHERF1 and P-ERMs with CFTR through PKCε phosphorylation. Moreover a reduction of the interaction between intracellular CFTR and the Golgi associated protein, CAL was observed following VIP stimulation. Silencing either ERMs or NHERF1 with siRNA prevented the VIP ability to increase CFTR surface expression and function, confirming that NHERF1 and P-ERMs are necessary for VIP regulation of the sustained activity of membrane CFTR. This study shows the cellular mechanism by which prolonged VIP stimulation of airway epithelial cells regulates CFTR-dependent secretions.en_US
dc.identifier.urihttp://hdl.handle.net/10222/40665
dc.language.isoenen_US
dc.subjectCystic Fibrosis, Respiratory Physiology, VIP mechanism of actionen_US
dc.titleRegulation of CFTR Endocytosis by the Vasoactive Intestinal Peptide: Role of PKCεen_US

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