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Academic literature on the topic 'CFTR function'

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Published: 11 March 2023

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Journal articles on the topic "CFTR function"

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Bossard, Florian, Amal Robay, Gilles Toumaniantz, Shehrazade Dahimene, Frédéric Becq, Jean Merot, and Chantal Gauthier. "NHE-RF1 protein rescues ΔF508-CFTR function." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 5 (May 2007): L1085—L1094. http://dx.doi.org/10.1152/ajplung.00445.2005.

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In cystic fibrosis (CF), the ΔF508-CFTR anterograde trafficking from the endoplasmic reticulum to the plasma membrane is inefficient. New strategies for increasing the delivery of ΔF508-CFTR to the apical membranes are thus pathophysiologically relevant targets to study for CF treatment. Recent studies have demonstrated that PDZ-containing proteins play an essential role in determining polarized plasma membrane expression of ionic transporters. In the present study we have hypothesized that the PDZ-containing protein NHE-RF1, which binds to the carboxy terminus of CFTR, rescues ΔF508-CFTR expression in the apical membrane of epithelial cells. The plasmids encoding ΔF508-CFTR and NHE-RF1 were intranuclearly injected in A549 or Madin-Darby canine kidney (MDCK) cells, and ΔF508-CFTR channel activity was functionally assayed using SPQ fluorescent probe. Cells injected with ΔF508-CFTR alone presented a low chloride channel activity, whereas its coexpression with NHE-RF1 significantly increased both the basal and forskolin-activated chloride conductances. This last effect was lost with ΔF508-CFTR deleted of its 13 last amino acids or by injection of a specific NHE-RF1 antisense oligonucleotide, but not by NHE-RF1 sense oligonucleotide. Immunocytochemical analysis performed in MDCK cells transiently transfected with ΔF508-CFTR further revealed that NHE-RF1 specifically determined the apical plasma membrane expression of ΔF508-CFTR but not that of a trafficking defective mutant potassium channel (KCNQ1). These data demonstrate that the modulation of the expression level of CFTR protein partners, like NHE-RF1, can rescue ΔF508-CFTR activity.
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Borkenhagen, Beatrice, and Peter Prehm. "Recovery of ΔF508-CFTR Function by Citrate." Nutrients 14, no. 20 (October 14, 2022): 4283. http://dx.doi.org/10.3390/nu14204283.

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Treatment of cystic fibrosis relies so far on expensive and sophisticated drugs. A logical approach to rescuing the defective ΔF508-CFTR protein has not yet been published. Therefore, virtual docking of ATP and CFTR activators to the open conformation of the CFTR protein was performed. A new ATP binding site outside of the two known locations was identified. It was located in the cleft between the nucleotide binding domains NBD1 and NBD2 and comprised six basic amino acids in close proximity. Citrate and isocitrate were also bound to this site. Citrate was evaluated for its action on epithelial cells with intact CFTR and defective ΔF508-CFTR. It activated hyaluronan export from human breast carcinoma cells and iodide efflux, and recovered ΔF508-CFTR from premature intracellular degradation. In conclusion, citrate is an activator for ΔF508-CFTR and increases export by defective ΔF508-CFTR into the extracellular matrix of epithelial cells.
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BRADBURY, NEIL A. "Intracellular CFTR: Localization and Function." Physiological Reviews 79, no. 1 (January 1, 1999): S175—S191. http://dx.doi.org/10.1152/physrev.1999.79.1.s175.

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Bradbury, Neil A. Intracellular CFTR: Localization and Function. Physiol. Rev. 79, Suppl.: S175–S191, 1999. — There is considerable evidence that CFTR can function as a chloride-selective anion channel. Moreover, this function has been localized to the apical membrane of chloride secretory epithelial cells. However, because cystic fibrosis transmembrane conductance regulator (CFTR) is an integral membrane protein, it will also be present, to some degree, in a variety of other membrane compartments (including endoplasmic reticulum, Golgi stacks, endosomes, and lysosomes). An incomplete understanding of the molecular mechanisms by which alterations in an apical membrane chloride conductance could give rise to the various clinical manifestations of cystic fibrosis has prompted the suggestion that CFTR may also play a role in the normal function of certain intracellular compartments. A variety of intracellular functions have been attributed to CFTR, including regulation of membrane vesicle trafficking and fusion, acidification of organelles, and transport of small anions. This paper aims to review the evidence for localization of CFTR in intracellular organelles and the potential physiological consequences of that localization.
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Carroll, Tiziana Piazza, Erik M. Schwiebert, and William B. Guggino. "CFTR: Structure and Function." Cellular Physiology and Biochemistry 3, no. 5-6 (1993): 388–99. http://dx.doi.org/10.1159/000154700.

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Meng, Xin, Jack Clews, Anca D. Ciuta, Eleanor R. Martin, and Robert C. Ford. "CFTR structure, stability, function and regulation." Biological Chemistry 400, no. 10 (October 25, 2019): 1359–70. http://dx.doi.org/10.1515/hsz-2018-0470.

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Abstract Cystic fibrosis transmembrane conductance regulator (CFTR) is a unique member of the ATP-binding cassette family of proteins because it has evolved into a channel. Mutations in CFTR cause cystic fibrosis, the most common genetic disease in people of European origin. The F508del mutation is found in about 90% of patients and here we present data that suggest its main effect is on CFTR stability rather than on the three-dimensional (3D) folded state. A survey of recent cryo-electron microscopy studies was carried out and this highlighted differences in terms of CFTR conformation despite similarities in experimental conditions. We further studied CFTR structure under various phosphorylation states and with the CFTR-interacting protein NHERF1. The coexistence of outward-facing and inward-facing conformations under a range of experimental conditions was suggested from these data. These results are discussed in terms of structural models for channel gating, and favour the model where the mostly disordered regulatory-region of the protein acts as a channel plug.
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Ramalho, Anabela S., Eva Fürstová, Annelotte M. Vonk, Marc Ferrante, Catherine Verfaillie, Lieven Dupont, Mieke Boon, et al. "Correction of CFTR function in intestinal organoids to guide treatment of cystic fibrosis." European Respiratory Journal 57, no. 1 (August 3, 2020): 1902426. http://dx.doi.org/10.1183/13993003.02426-2019.

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RationaleGiven the vast number of cystic fibrosis transmembrane conductance regulator (CFTR) mutations, biomarkers predicting benefit from CFTR modulator therapies are needed for subjects with cystic fibrosis (CF).ObjectivesTo study CFTR function in organoids of subjects with common and rare CFTR mutations and evaluate correlations between CFTR function and clinical data.MethodsIntestinal organoids were grown from rectal biopsies in a cohort of 97 subjects with CF. Residual CFTR function was measured by quantifying organoid swelling induced by forskolin and response to modulators by quantifying organoid swelling induced by CFTR correctors, potentiator and their combination. Organoid data were correlated with clinical data from the literature.ResultsAcross 28 genotypes, residual CFTR function correlated (r2=0.87) with sweat chloride values. When studying the same genotypes, CFTR function rescue by CFTR modulators in organoids correlated tightly with mean improvement in lung function (r2=0.90) and sweat chloride (r2=0.95) reported in clinical trials. We identified candidate genotypes for modulator therapy, such as E92K, Q237E, R334W and L159S. Based on organoid results, two subjects started modulator treatment: one homozygous for complex allele Q359K_T360K, and the second with mutation E60K. Both subjects had major clinical benefit.ConclusionsMeasurements of residual CFTR function and rescue of function by CFTR modulators in intestinal organoids correlate closely with clinical data. Our results for reference genotypes concur with previous results. CFTR function measured in organoids can be used to guide precision medicine in patients with CF, positioning organoids as a potential in vitro model to bring treatment to patients carrying rare CFTR mutations.
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Londino, James D., Ahmed Lazrak, Asta Jurkuvenaite, James F. Collawn, James W. Noah, and Sadis Matalon. "Influenza matrix protein 2 alters CFTR expression and function through its ion channel activity." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 9 (May 1, 2013): L582—L592. http://dx.doi.org/10.1152/ajplung.00314.2012.

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The human cystic fibrosis transmembrane conductance regulator (CFTR) is a cyclic AMP-activated chloride (Cl−) channel in the lung epithelium that helps regulate the thickness and composition of the lung epithelial lining fluid. We investigated whether influenza M2 protein, a pH-activated proton (H+) channel that traffics to the plasma membrane of infected cells, altered CFTR expression and function. M2 decreased CFTR activity in 1) Xenopus oocytes injected with human CFTR, 2) epithelial cells (HEK-293) stably transfected with CFTR, and 3) human bronchial epithelial cells (16HBE14o−) expressing native CFTR. This inhibition was partially reversed by an inhibitor of the ubiquitin-activating enzyme E1. Next we investigated whether the M2 inhibition of CFTR activity was due to an increase of secretory organelle pH by M2. Incubation of Xenopus oocytes expressing CFTR with ammonium chloride or concanamycin A, two agents that alkalinize the secretory pathway, inhibited CFTR activity in a dose-dependent manner. Treatment of M2- and CFTR-expressing oocytes with the M2 ion channel inhibitor amantadine prevented the loss in CFTR expression and activity; in addition, M2 mutants, lacking the ability to transport H+, did not alter CFTR activity in Xenopus oocytes and HEK cells. Expression of an M2 mutant retained in the endoplasmic reticulum also failed to alter CFTR activity. In summary, our data show that M2 decreases CFTR activity by increasing secretory organelle pH, which targets CFTR for destruction by the ubiquitin system. Alteration of CFTR activity has important consequences for fluid regulation and may potentially modify the immune response to viral infection.
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Taylor-Cousar, Jennifer L., Marcus A. Mall, Bonnie W. Ramsey, Edward F. McKone, Elizabeth Tullis, Gautham Marigowda, Charlotte M. McKee, et al. "Clinical development of triple-combination CFTR modulators for cystic fibrosis patients with one or two F508del alleles." ERJ Open Research 5, no. 2 (April 2019): 00082–2019. http://dx.doi.org/10.1183/23120541.00082-2019.

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Cystic fibrosis (CF) is caused by mutations in the CF transmembrane conductance regulator gene (CFTR) that result in diminished quantity and/or function of the CFTR anion channel. F508del-CFTR, the most common CF-causing mutation (found in ∼90% of patients), causes severe processing and trafficking defects, resulting in decreased CFTR quantity and function. CFTR modulators are medications that increase the amount of mature CFTR protein (correctors) or enhance channel function (potentiators) at the cell surface.Combinations of CFTR correctors and potentiators (i.e. lumacaftor/ivacaftor, tezacaftor/ivacaftor) have demonstrated clinical benefit in subsets of patients. However, none are approved for patients with CF heterozygous for F508del-CFTR and a minimal function mutation, i.e. a mutation that produces either no protein or protein that is unresponsive to currently approved CFTR modulators. Next-generation CFTR correctors VX-659 and VX-445, each in triple combination with tezacaftor and ivacaftor, improve CFTR processing, trafficking and function in vitro and have demonstrated clinical improvements in phase 2 studies in patients with CF with one or two F508del-CFTR alleles.Here, we present the rationale and design of four randomised phase 3 studies, and their open-label extensions, evaluating VX-659 (ECLIPSE) or VX-445 (AURORA) plus tezacaftor and ivacaftor in patients with one or two F508del-CFTR alleles.
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Maitra, Rangan, Perumal Sivashanmugam, and Keith Warner. "A Rapid Membrane Potential Assay to Monitor CFTR Function and Inhibition." Journal of Biomolecular Screening 18, no. 9 (May 7, 2013): 1132–37. http://dx.doi.org/10.1177/1087057113488420.

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The cystic fibrosis transmembrane conductance regulator (CFTR) protein is an important regulator of ion transport and fluid secretion in humans. Mutations to CFTR cause cystic fibrosis, which is a common recessive genetic disorder in Caucasians. Involvement of CFTR has been noted in other important diseases, such as secretory diarrhea and polycystic kidney disease. The assays to monitor CFTR function that have been described to date either are complicated or require specialized instrumentation and training for execution. In this report, we describe a rapid FlexStation-based membrane potential assay to monitor CFTR function. In this assay, agonist-mediated activation of CFTR results in membrane depolarization that can be monitored using a fluorescent membrane potential probe. Availability of a simple mix-and-read assay to monitor the function of this important protein might accelerate the discovery of CFTR ligands to study a variety of conditions.
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Bertrand, Carol A., and Raymond A. Frizzell. "The role of regulated CFTR trafficking in epithelial secretion." American Journal of Physiology-Cell Physiology 285, no. 1 (July 2003): C1—C18. http://dx.doi.org/10.1152/ajpcell.00554.2002.

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The focus of this review is the regulated trafficking of the cystic fibrosis transmembrane conductance regulator (CFTR) in distal compartments of the protein secretory pathway and the question of how changes in CFTR cellular distribution may impact on the functions of polarized epithelial cells. We summarize data concerning the cellular localization and activity of CFTR and attempt to synthesize often conflicting results from functional studies of regulated endocytosis and exocytosis in CFTR-expressing cells. In some instances, findings that are inconsistent with regulated CFTR trafficking may result from the use of overexpression systems or nonphysiological experimental conditions. Nevertheless, judging from data on other transporters, an appropriate cellular context is necessary to support regulated CFTR trafficking, even in epithelial cells. The discovery that disease mutations can influence CFTR trafficking in distal secretory and recycling compartments provides support for the concept that regulated CFTR recycling contributes to normal epithelial function, including the control of apical CFTR channel density and epithelial protein secretion. Finally, we propose molecular mechanisms for regulated CFTR endocytosis and exocytosis that are based on CFTR interactions with other proteins, particularly those whose primary function is membrane trafficking. These models provide testable hypotheses that may lead to elucidation of CFTR trafficking mechanisms and permit their experimental manipulation in polarized epithelial cells.
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Dissertations / Theses on the topic "CFTR function"

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Fisher, John T. "Ferret CFTR processing and function." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3453.

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The most common cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation is δF508 and this causes cystic fibrosis (CF). Animal models that recapitulate the human disease phenotype are critical to understanding pathophysiologic mechanisms in CF and developing therapies. New CF models in the pig and ferret have been generated that develop lung, pancreatic, liver, and intestinal pathologies that reflect disease in CF patients. Species-specific biology in the processing of CFTR has demonstrated that pig and mouse δF508-CFTR proteins are more effectively processed to the apical membrane of airway epithelia than human δF508-CFTR. The processing behavior of ferret wild-type (WT) and δF508-CFTR proteins remain unknown and such information is important to predicting the utility of a δF508-CFTR ferret. To this end, we sought to compare processing, membrane stability, and function of human and ferret WT- and δF508-CFTR proteins in a heterologous expression system using HT1080, HEK293T, BHK21, and Cos7 cells, as well as human and ferret CF polarized airway epithelia. Analysis of the protein processing and stability by metabolic pulse-chase and surface On-Cell Western blots revealed that WT-fCFTR half-life and membrane stability were increased relative to WT-hCFTR. Furthermore, in BHK21, Cos7, and CuFi cells, human and ferret δF508-CFTR processing was negligible, while low levels of processing of δF508-fCFTR could be seen in HT1080 and HEK293T cells. Only the WT-fCFTR, but not δF508-fCFTR, produced functional cAMP-inducible chloride currents in both CF human and ferret airway epithelia. Further elucidation of the mechanism responsible for elevated fCFTR protein stability may lead to new therapeutic approaches to augment CFTR function. These findings also suggest that generation of a ferret CFTRδF508/δF508 animal model may be useful. Furthermore, in the CFTR and CFTR+/+ ferret model we have characterized abnormalities in the bioelectric properties of the trachea, stomach, intestine and gallbladder of newborn CF ferrets. Short circuit current (ISC) analysis of CF and WT tracheas revealed the following similarities and differences: 1) amiloride sensitive sodium currents were similar between genotypes, 2) responses to 4,4'-diisothiocyano-2,2'-stilbene disulphonic acid (DIDS) were ~4-fold greater in CF animals, suggesting elevated baseline chloride transport through non-CFTR channels, and 3) as expected, there was a lack of IBMX/forskolin-stimulated and GlyH-101-inhibited currents in CF animals due to the lack of CFTR. CFTR mRNA and protein was present throughout all levels of the WT ferret and IBMX/forskolin-inducible ISC was only observed in WT animals. Interestingly, IBMX/forskolin-inducible intestinal ISC in WT animals was not inhibited by the CFTR inhibitor GlyH-101 or bumetanide. The luminal pH of the CF ferret stomach was significantly decreased relative to the controls, while both genotypes maintained near neutral pH along the length of the intestine. The WT stomach and gallbladder exhibited significantly enhanced IBMX/forskolin ISC responses and inhibition by GlyH-101 relative to CF samples. These findings demonstrate that multiple organs affected by disease in the CF ferret have bioelectric abnormalities consistent with the lack of cAMP-mediated chloride transport.
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Williams, M. T. S. "Impact of different CFTR Mutations on Airway Epithelium Function." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527902.

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Scholl, Daniel. "Exchange between ordered and disordered segments in CFTR modulates function at the expense of stability: A molecular pathway for misfolding of CFTR." Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/313253.

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The genetic disease cystic fibrosis is the most common lethal genetic disease in Western countries. People born with cystic fibrosis suffer from many health issues including severe respiratory problems, inflammation and recurrent lung infections that can become fatal. The disease is caused by the loss of function of a protein called the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR is an chloride ion channel and, in healthy people, its activity assures correct water and salt transport across the cell membrane. Most cases of cystic fibrosis are caused by a genetic defect that leads to the deletion of phenylalanine 508 (F508del) in the amino acid sequence of the protein. The molecular mechanism by which F508del leads to loss of function of the CFTR channel is still poorly understood. The mutation is found in the first nucleotide binding domain (NBD1) and studies have shown that it causes misfolding of CFTR and subsequent degradation of the protein by the cellular quality control system. It is established that the mutation affects stability and dynamics of NBD1 but does not alter its structure significantly. This destabilizing effect of F508del can be compensated by specific mutations distributed over different regions of NBD1, leading to recovery of membrane expression of a functional channel. A surprising example involves the regulatory insertion (RI), a 32-residue long segment found in all CFTR orthologs but not in related channels or transporters. The RI is not resolved in crystal structures of NBD1 nor cryo-EM structures of CFTR and has been described as intrinsically disordered. Its functional role in CFTR is unknown. Removal of the RI increases the stability of the NBD1 domain and, in the context of F508del-CFTR, this deletion restores maturation, cell surface expression and activity of the mutant channel. We probed the effect of the RI on NBD1 structure, dynamics and allostery using X-ray crystallography, single molecule FRET and hydrogen-deuterium exchange. We discovered that the RI enables an alternative NBD1 fold which departs markedly from the canonical fold previously observed for this domain and the NBDs of other ABC transporters. The conformational equilibrium between these states is regulated by ATP binding and affected by disease-associated conditions. Aside from clear alterations to structure and dynamics of NBD1, the RI also affects allostery, i.e. how NBD1 structure and dynamics respond to perturbations such as ligand binding. Finally, we show that the RI-enabled conformation is adopted in full-length CFTR and associated with increased channel activity in electrophysiological assays. We then identify an allosteric network that links the structural hotspots of the conformational changes to F508 and its surroundings. Lastly, we argue that these conformational changes lead to unfolding of NBD1 in the context of F508del, providing a new model for the molecular mechanism leading to pathogenesis.
Doctorat en Sciences
info:eu-repo/semantics/nonPublished
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Jurkuvenaite, Asta. "Biogenesis, trafficking, and function of wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR)." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/jurkuvenaite.pdf.

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Hughes, Lauren Kimberley. "Investigation of anion transport by artificial ionophores to bypass loss of CFTR function in cystic fibrosis." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442200.

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MANCINI, GIULIA. "GANGLIOSIDE GM1 AS ADJUVANT FOR ORKAMBI® THERAPY TO RESTORE PLASMA MEMBRANE STABILITY AND FUNCTION OF F508DEL-CFTR." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/604127.

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Cystic fibrosis (CF) is the most common, fatal genetic disease in the Caucasian population caused by loss of function mutations in gene encoding for the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR is expressed at the apical surface of epithelial cells of different organs, such as: lungs, pancreas, gut, and testes. For this reason even if in CF the pulmonary manifestations are the most severe, CF is considered a multi-system disease, which affects several bodily districts. The new challenge for the CF therapy is based on the development of small molecules able to rescue the function of the mutated CFTR. Many pharmacological agents have been designed to increase the surface level of mutated CFTR (correctors), as well as its plasma membrane (PM) activity (potentiators). Recently, combined therapy that includes a corrector of the CFTR folding (lumacaftor or VX-809) and a potentiator of the channel activity (ivacaftor or VX-770) called Orkambi®, was approved for CF patients homozygous for the deletion of phenylalanine at position 508 (F508del), the most common CF-causing mutation. Unfortunately, clinical studies revealed that the effects of Orkambi® on lung function were modest, due to low stability of rescued F508del-CFTR at the PM level. Indeed, many factors contribute to PM CFTR stability, including its compartmentalization in PM macromolecular complexes composed of phospholipids, sphingolipids, with particular regards for monosialoganglioside 1 (GM1), and scaffolding proteins such as ezrin and NHERF-1. Interestingly, it has been proved that in bronchial epithelial cells the lack of CFTR in the cell PM, such as in the case of the patients carrying the mutation F508del, is associated with a decreased content of GM1. By performing photolabelling experiments, I demonstrated for the first time that GM1 and CFTR at PM level reside in the same microdomain, suggesting a direct interaction between them. Then I investigated on the potential effect of the exogenous administration of ganglioside GM1 on the PM stabilization and function of F508del-CFTR rescued by Orkambi® treatment. In particular, I proved that in CF bronchial epithelial cells GM1 antagonizes the negative effect of VX-770, increasing F508del-CFTR maturation and its channel activity by the recruitment of the scaffolding proteins NHERF-1 and ezrin. Taken together the results obtained during my PhD project pointed out the role of GM1 as possible adjuvant to Orkambi® therapy to restore the function of F508del-CFTR.
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Harman, Katharine. "Exploring the relationship between loss of CFTR protein function and markers of disease severity in chronic suppurative lung disease." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/57500.

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Cystic fibrosis (CF) and Primary Ciliary Dyskinesia (PCD) are chronic suppurative lung diseases (CSLD). CF is characterised by inherited mutations affecting the cystic fibrosis transmembrane regulator (CFTR) protein, which is thought to be normal in PCD, however the role of CFTR in disease is incompletely understood. This thesis investigates the relationship between CFTR, inflammation and airway health, firstly in the context of the CF gene therapy Multidose trial followed by contrasting CF, PCD and control patients. The first study explored the relationship between lower airway potential difference (LAPD) measurements performed in the Multidose trial as a measure of CFTR function, and physiological, radiographic and inflammatory markers of disease severity. At baseline, FEV1 correlated with basal LAPD measurements, however not between restored chloride secretion and change in airway disease following treatment; implicating the role of sodium transport, not chloride in disease pathogenesis. As no direct correlation was seen, I went on to explore an alternative theory that a bi-directional relationship exists between CFTR and inflammation; CFTR dysfunction triggers a hyper-inflammatory state and inflammation causes secondary CFTR dysfunction. Cell cultures were cultivated from the nasal epithelium of patients with CF, PCD and controls. Both at baseline and following stimulation with common respiratory pathogens, the levels of inflammatory mediators in the supernatant from each group of cells were comparable. The numbers involved with this study were small, however did not indicate that CF cells cultured in these conditions (in vitro) were hyper-inflammatory. The final study explored in vivo whether inflammation causes secondary CFTR dysfunction. Nasal potential difference (NPD) measurements were compared with localised levels of inflammation in subjects with CF, PCD and controls. PCD traces showed reduced chloride secretion, however it was not possible to differentiate secondary CFTR dysfunction from damage to epithelial cell integrity. Elevated levels of inflammatory mediators were detected in PCD nasal fluid, however the results were variable and these levels did not correlate with NPD measurements of ion channel function. These studies did not support the hypothesis that there is a direct relationship between CFTR function and airway disease, that in vitro CF cells are hyperinflammatory, or in vivo that inflammation leads to secondary CFTR dysfunction. The experiments performed in this thesis provide a basis for future work exploring this relationship, and may help guide future trials for novel therapies in CF.
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Sedin, John. "Prevention of Postoperative Duodenal Ileus by COX-2 Inhibition Improves Duodenal Function in Anaesthetised Rats." Doctoral thesis, Uppsala universitet, Fysiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-198049.

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Abdominal surgery inhibits gastrointestinal motility, a phenomenon referred to as postoperative ileus. Since the postoperative ileus disturbs duodenal physiology it is important to minimize the side effects of this condition. Recent experiments in our laboratory show that treatment of anaesthetised rats with parecoxib, a selective cyclooxygenase-2 inhibitor, prevents duodenal postoperative ileus, increases duodenal mucosal bicarbonate secretion and improves other functions as well. One aim of the thesis was to investigate whether removal of luminal chloride affect the parecoxib- and the vasoactive intestinal peptide (VIP)-induced stimulation of duodenal mucosal bicarbonate secretion. The proximal duodenum of anaesthetised Dark Agouti rats was perfused with isotonic solutions containing zero or low Cl- and the effect on luminal alkalinisation determined. The basal as well as the parecoxib-induced increase in alkalinisation, but not that stimulated by VIP, were markedly reduced in the absence of luminal Cl-. One important function of the duodenum is to adjust luminal osmolality towards that in the blood. It is believed that the adjustment of osmolality in the duodenum is achieved by osmosis and diffusion of electrolytes along their concentration gradients and that these processes occur predominately paracellularly. Another aim of the thesis was to examine whether prevention of postoperative ileus affects the duodenal response to luminal hypertonicity. The proximal duodenum of anaesthetised Dark Agouti and Sprague-Dawley rats were perfused with hypertonic solutions of different composition and osmolality and the effects on duodenal motility, alkaline secretion, transepithelial fluid flux, mucosal permeability and the adjustment of luminal osmolality were determined in absence and presence of parecoxib. It is concluded that COX-2 inhibition increases duodenal mucosal bicarbonate secretion by stimulating apical Cl-/HCO3- exchange in duodenocytes. Furthermore, pretreatment of anaesthetised rats with parecoxib improves a number of duodenal functions in both rat strains that contribute to improve the ability to adjust luminal osmolality. The choice of rat strain is another important feature to consider when interpreting the results because the DA strain was more responsive to luminal hypertonicity than the SD strain. Finally, several evidences are provided to suggest that the adjustment of luminal osmolality in the rat duodenum is a regulated process.
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Foxx-Lupo, William T., and Eric M. Snyder. "Influence of Genetic Variation of the Alpha-Subunit of the Epithelial Sodium Channel (ENaC) on Baseline Pulmonary Function and Exhaled Sodium Ions (Na+) and Chloride Ions (Cl-) in Healthy Subjects and Patients with Cystic Fibrosis." The University of Arizona, 2012. http://hdl.handle.net/10150/614485.

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Class of 2012 Abstract
Specific Aims: The epithelial sodium channels (ENaC) found on the apical membranes of epithelial cells including those lining the respiratory tract are the rate limiting step of the absorption of excess fluid from the airspace of the alveoli. ENaC function is modulated by the effects of various physiologic signals such as the adrenergic and purinergic pathways, in addition to other local channels which control the flow of negatively charged ions such as the cystic fibrosis transmembrane conductance regulator (CFTR). We sought to determine the influence of genetic variation on the alpha subunit of ENaC at amino acid position 663 on baseline exhaled ions and pulmonary function in patients with CF. Methods: We assessed pulmonary function ( forced vital capacity[FVC], forced expiratory volume in one second [FEV1], forced expiratory flow maximum[FEFmax]) using a Medical Graphics cardiopulmonary testing device (Minneapolis, MN). Measures of exhaled sodium (Na+) and chloride (Cl-) were obtained using exhaled breathe condensate collected on a Jaeger Ecoscreen condenser unit (Cardinal Health, Yorba Linda, CA) with Na+ quantification using an atomic absorption spectrophotometer (Analyst 100; Perkin Elmer, Norwalk, CT) and Cl- anion quantification using a Dionex AS11 HC column. Healthy n=31 (n=18[58%], 9[29%], and 4[13%] subjects; Body mass index (BMI)=23±1, 25±2, and 25±2kg/ m2 for AA, AT and TT groups respectively). CF n= 42 (n=33[79%], 7[16%], and 2[5%] subjects; BMI equals 23±7, 19±0.4, and 20±2.2kg/m2 for AA, AT and TT groups respectively). Main Results: We found that the distribution of genotypes in CF differed from healthy subjects, with the AA genotype in 80% of CF and 59% in healthy. No significant difference were demonstrated in healthy subjects between genotype groups for pulmonary function and exhaled chloride while the genotypes did differ in exhaled Na (Na=2.9±0.4, 1.7±0.3, and 3.7±1.1mmol/L for AA, AT, and TT respectively, ANOVA p=0.07). CF subjects with the AA genotype had a higher baseline exhaled Cl-, FEV1, and FEFmax than those in the AA group (Cl=0.125±0.038,0.0 27±0.007, and 0.033±0.02 mmol/L ; FEV1=71±5, 68±11, and 40±22L; FEFmax=86±4, 72±7, and 44±24L/sec; for AA, AT, and TT respectively, ANOVA p<0.05, Tukey [AA vs. TT] p<0.05) while exhaled Na+ and FVC were similar between genotypes. Conclusions: Our results suggest that CF subjects with the AA genotype of the alpha subunit of the ENaC have a higher baseline exhaled Cl- and a resulting increase in pulmonary function when compared to the overactive TT groupCF patients with the TT αENaC genotype are likely candidates for early identification and treatment with inhaled ENaC inhibitors or other modulators of this pathway in order to improve survival.
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Matusis, Alec (Alec L. ). 1971. "CFT correlation functions from AdS/CFT correspondence." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85332.

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Books on the topic "CFTR function"

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Nieto, Juan Miguel. Spinning Strings and Correlation Functions in the AdS/CFT Correspondence. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96020-3.

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United States. Congress. House. Committee on Energy and Commerce. Subcommittee on Telecommunications and Finance. SEC/CFTC jurisdictional issues: Hearings before the Subcommittee on Telecommunications and Finance of the Committee on Energy and Commerce, House of Representatives, One Hundred First Congress, second session, on H.R. 4477, a bill to combine the functions of the Commodity Futures Trading Commission and the Securities and Exchange Commission ... May 3 and 24, 1990. Washington: U.S. G.P.O., 1990.

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Farinha, Carlos M. M. CFTR and Cystic Fibrosis: From Structure to Function. Springer, 2017.

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Cao, Lishuang. Modulation of Cftr & Enac Channel Function by Interacting Proteins & Trafficking. Leuven University Press, 2005.

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Kogan, Ilana. Regulation and function of the cystic fibrosis transmembrane conductance regulator (CFTR). 2003.

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Wei, Lin. Electrophysiological Studies of Cftr Function: Effects of Cftr Mutations and Interactions With Other Chloride Channels (Acta Biomedica Lovaniensia, 236). Leuven Univ Pr, 2001.

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Snell, Jamey, and Thomas J. Mancuso. Cystic Fibrosis. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0023.

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Cystic fibrosis (CF) is an inherited, autosomal recessive, multisystem disease. Dysfunction of the cystic fibrosis transmembrane conductance regulator protein (CFTR) in epithelial cells is the primary defect in CF. Defects in CFTR are the cause for lung disease, exocrine pancreatic insufficiency and failure, male infertility, and liver disease. CF can present with a variety of respiratory and gastrointestinal signs, including meconium ileus in the newborn period, hypernatremic dehydration, pulmonary insufficiency, nasal polyps, and insulin-dependent diabetes mellitus. As affected children grow, dysfunction in CFTR leads to chronic and progressive lung disease, characterized by suppurative infection and the development of bronchiectasis. CFTR dysfunction also affects exocrine function, leading to pancreatic insufficiency, malabsorption, and growth failure. In the past, history and physical exam with sweat chloride testing were the cornerstones of diagnosis. Diagnosis is now made with the newborn screening test for immunoreactive trypsinogen.
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Taylor, Christopher, and Sally Connolly. Gastrointestinal disease and nutrition. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0007.

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This chapter discusses the common gastrointestinal and nutritional consequences of cystic fibrosis (CF) including hepato-biliary disease. The pathophysiology of obstructive gut disease (meconium ileus and distal ileal obstruction) is discussed with reference to CFTR dysfunction. The diagnosis and management of gastro-oesophageal reflux, an increasingly common problem in both children and adults with CF, is also considered in some depth. A new section on eosinophilic gut disease has been added. The importance of nutrition in maintaining lung function is emphasized with a section on pancreatic enzyme physiology and guidance on optimizing pancreatic enzyme replacement therapy. An investigation plan to exclude concomitant gut disease for a child with poor weight gain is given, together with a section on invasive nutritional support. The diagnosis of hepatic disease and biliary complications is considered together with suggested treatments and a long-term monitoring plan
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Edenborough, Frank P. Fertility, contraception, and pregnancy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0012.

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This chapter describes the physiological effect of CFTR dysfunction on the development of the reproductive system. Young people with CF and their parents are poorly educated regarding sexual function and becoming parents themselves. They often wish to learn this from their CF teams. Male and female potency, reproductive genetics, and the need for genetic and general counselling before embarking on pregnancy are covered. Contraception, emphasizing the need to avoid unwanted pregnancy and sexually transmitted diseases, and assisted reproductive techniques are described. We discuss the evolving medical and obstetric management of pregnancy, including the likely need for optimizing drug treatment or escalating to more intensive treatment for intercurrent infection. Optimal delivery in the context of maternal health, fetal risks, and longer term maternal outcomes are discussed. Pregnancy post transplantation and termination of unwanted pregnancy or where the mother is too poorly to continue conclude the chapter.
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Kriemler, Susi. Exercise, physical activity, and cystic fibrosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0033.

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Cystic fibrosis (CF) is the most common genetic autosomal recessive disease of the Caucasian race, generally leading to death in early adulthood.1 The frequency of the gene carrier (heterozygote) is 1:20–25 in Caucasian populations, 1:2000 in African-Americans, and practically non-existent in Asian populations. The disease occurs in about 1 in every 2500 life births of the white population. Mean survival has risen from 8.4 years in 1969 to 32 years in 2000 due to improvements in treatment. The genetic defect causes a pathological electrolyte transport through the cell membranes by a defective chloride channel membrane transport protein [cystic fibrosis transmembrane conductance regulator (CFTR)]. With respect to the function, this affects mainly the exocrine glands of secretory cells, sinuses, lungs, pancreas, liver, and the reproductive tract of the human body leading to a highly viscous, water-depleted secretion. The secretion cannot leave the glands and in consequence causes local inflammation and destruction of various organs. The main symptoms include chronic inflammatory pulmonary disease with a progressive loss of lung function, exocrine and sometimes endocrine pancreas insufficiency, and an excessive salt loss through the sweat glands.1 A summary of the signs and symptoms of CF will be given with a special emphasis on the effect of exercise performance and capacity.
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Book chapters on the topic "CFTR function"

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Chen, Jeng-Haur, Zhiwei Cai, Hongyu Li, and David N. Sheppard. "Function of CFTR Protein: Ion Transport." In Cystic Fibrosis in the 21st Century, 38–44. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000088472.

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Gill, Deborah, and Janet E. Larson. "Function of CFTR Protein: Developmental Role." In Cystic Fibrosis in the 21st Century, 54–60. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000088474.

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Almaça, Joana, Shehrazade Dahimène, Nicole Appel, Christian Conrad, Karl Kunzelmann, Rainer Pepperkok, and Margarida D. Amaral. "Functional Genomics Assays to Study CFTR Traffic and ENaC Function." In Methods in Molecular Biology, 249–64. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-120-8_15.

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Kunzelmann, Karl. "Introduction to Section V: Assessment of CFTR Function." In Methods in Molecular Biology, 407–18. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-117-8_26.

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Nissim-Rafinia, Malka, and Batsheva Kerem. "Splicing Modulation as a Modifier of the CFTR Function." In Alternative Splicing and Disease, 233–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/978-3-540-34449-0_10.

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Cheng, Hwee Ming, Kin Kheong Mah, and Kumar Seluakumaran. "Pancreatic Exocrine Function: Pancreatic Ductal Cell, CFTR Chloride Channel. Secretin." In Defining Physiology: Principles, Themes, Concepts. Volume 2, 57–58. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-62285-5_16.

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Verkman, A. S., and Luis J. V. Galietta. "In Vitro/Ex Vivo Fluorescence Assays of CFTR Chloride Channel Function." In Cystic Fibrosis in the 21st Century, 93–101. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000088486.

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Loo, Tip W., and David M. Clarke. "Repair of CFTR Folding Defects with Correctors that Function as Pharmacological Chaperones." In Methods in Molecular Biology, 23–37. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-117-8_3.

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Griesenbach, Uta, Felix M. Munkonge, Stephanie Sumner-Jones, Emma Holder, Stephen N. Smith, A. Christopher Boyd, Deborah R. Gill, Stephen C. Hyde, David Porteous, and Eric W. F. W. Alton. "Assessment of CFTR Function after Gene Transfer In Vitro and In Vivo." In Methods in Molecular Biology, 229–42. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-237-3_14.

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Van Goor, Fredrick, Sabine Hadida, and Peter Grootenhuis. "Pharmacological Rescue of Mutant CFTR Function for the Treatment of Cystic Fibrosis." In Topics in Medicinal Chemistry, 91–120. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/7355_2008_022.

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Conference papers on the topic "CFTR function"

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Stanford, D., L. W. Rasmussen, J. LaFontaine, A. Allen, E. L. Burnham, and S. V. Raju. "Roflumilast Reverses Alcohol Impairment of CFTR Function and Mucus Clearance." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1896.

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Martinovich, Kelly, Anthony Kicic, Sue Fletcher, Steve Wilton, and Steve Stick. "Rescue of CFTR function impaired by mutations in exon 15." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.361.

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Kneller, L., L. Erfinanda, W. M. Kuebler, M. Witzenrath, and B. Gutbier. "WNK1 signaling after loss of CFTR function in pneumonia-induced lung barrier failure." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1072.

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Stick, SM, EN Sutanto, AK Scaffidi, D. Fischer, and A. Kicic. "Efficient Restoration of dF508 CFTR Function in Primary Cystic Fibrosis Airway Epithelial Cells (AEC)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1770.

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Nguyen, J. P., R. D. Huff, Q. C. T. Cao, N. Tiessen, C. Carlsten, and J. A. Hirota. "Effects of Environmental Insults on CFTR Expression and Function in Human Airway Epithelial Cells." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4254.

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Grosse-Onnebrink, J., V. Mete, H. Omran, and W. M. Weber. "CFTR function in respiratory epithelial cell cultures: step to individualize treatments in cystic fibrosis?" In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3031.

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Gräber, Simon, Christian Dopfer, Lutz Naehrlich, Lena Gyulumyan, Heike Scheuermann, Stephanie Hirtz, Sabine Wege, et al. "Effects of Lumacaftor-Ivacaftor Therapy on CFTR Function in Phe508del Homozygous Patients with Cystic Fibrosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3415.

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Xu, Xin, Steven M. Rowe, Lijuan Fan, James A. Fortenberry, Yao Li, Mojtaba Abdul Roda, Paula Allan, John P. Clancy, and Amit Gaggar. "Role Of Protease Activated Receptor 2 In Human Neutrophil Elastase Mediated Modulation Of CFTR Function." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4161.

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Grosse-Onnebrink, Joerg, Vanessa Mete, Katharina Kolonko, Sandra Cindric, Simone Helms, Heymut Omran, and Wolf Michael Weber. "Measuring CFTR function in respiratory epithelial cell cultures: step to individualize treatments in cystic fibrosis?" In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa2669.

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Steinack, C., T. Gaisl, F. Beuschlein, S. Macé Matthew, and M. Ernst. "Triple CFTR modulator therapy is associated with improved endocrine pancreatic function in patients with cystic fibrosis." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3750.

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Reports on the topic "CFTR function"

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Hubbard, Sarah M., and Bryan Hubbard. Investigation of Strategic Deployment Opportunities for Unmanned Aerial Systems (UAS) at INDOT. Purdue University, 2020. http://dx.doi.org/10.5703/1288284317126.

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Unmanned aerial systems (UAS) are increasingly used for a variety of applications related to INDOT’s mission including bridge inspection, traffic management, incident response, construction and roadway mapping. UAS have the potential to reduce costs and increase capabilities. Other state DOTs and transportation agencies have deployed UAS for an increasing number of applications due to technology advances that provide increased capabilities and lower costs, resulting from regulatory changes that simplified operations for small UAS under 55 pounds (aka, sUAS). This document provides an overview of UAS applications that may be appropriate for INDOT, as well as a description of the regulations that affect UAS operation as described in 14 CFR Part 107. The potential applications were prioritized using Quality Function Deployment (QFD), a methodology used in the aerospace industry that clearly communicates qualitative and ambiguous information with a transparent framework for decision making. The factors considered included technical feasibility, ease of adoption and stakeholder acceptance, activities underway at INDOT, and contribution to INDOT mission and goals. Dozens of interviews with INDOT personnel and stakeholders were held to get an accurate and varied perspective of potential for UAVs at INDOT. The initial prioritization was completed in early 2019 and identified three key areas: UAS for bridge inspection safety as a part of regular operations, UAS for construction with deliverables provided via construction contracts, and UAS for emergency management. Descriptions of current practices and opportunities for INDOT are provided for each of these applications. An estimate of the benefits and costs is identified, based on findings from other agencies as well as projections for INDOT. A benefit cost analysis for the application of UAS for bridge inspection safety suggests a benefit cost over one for the analysis period.
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