Relevant bibliographies by topics / Cystic fibrosis transmembrane

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Cystic fibrosis transmembrane'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Cystic fibrosis transmembrane"

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Smith, Stephen S., Erich D. Steinle, Mark E. Meyerhoff, and David C. Dawson. "Cystic Fibrosis Transmembrane Conductance Regulator." Journal of General Physiology 114, no. 6 (November 29, 1999): 799–818. http://dx.doi.org/10.1085/jgp.114.6.799.

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The cystic fibrosis transmembrane conductance regulator (CFTR) Cl channel exhibits lyotropic anion selectivity. Anions that are more readily dehydrated than Cl exhibit permeability ratios (PS/PCl) greater than unity and also bind more tightly in the channel. We compared the selectivity of CFTR to that of a synthetic anion-selective membrane [poly(vinyl chloride)–tridodecylmethylammonium chloride; PVC-TDMAC] for which the nature of the physical process that governs the anion-selective response is more readily apparent. The permeability and binding selectivity patterns of CFTR differed only by a multiplicative constant from that of the PVC-TDMAC membrane; and a continuum electrostatic model suggested that both patterns could be understood in terms of the differences in the relative stabilization of anions by water and the polarizable interior of the channel or synthetic membrane. The calculated energies of anion–channel interaction, derived from measurements of either permeability or binding, varied as a linear function of inverse ionic radius (1/r), as expected from a Born-type model of ion charging in a medium characterized by an effective dielectric constant of 19. The model predicts that large anions, like SCN, although they experience weaker interactions (relative to Cl) with water and also with the channel, are more permeant than Cl because anion–water energy is a steeper function of 1/r than is the anion–channel energy. These large anions also bind more tightly for the same reason: the reduced energy of hydration allows the net transfer energy (the well depth) to be more negative. This simple selectivity mechanism that governs permeability and binding acts to optimize the function of CFTR as a Cl filter. Anions that are smaller (more difficult to dehydrate) than Cl are energetically retarded from entering the channel, while the larger (more readily dehydrated) anions are retarded in their passage by “sticking” within the channel.
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Akabas, Myles H. "Cystic Fibrosis Transmembrane Conductance Regulator." Journal of Biological Chemistry 275, no. 6 (February 11, 2000): 3729–32. http://dx.doi.org/10.1074/jbc.275.6.3729.

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Antoniu, Sabina Antonela. "Cystic fibrosis transmembrane regulator potentiators as promising cystic fibrosis therapies." Expert Opinion on Investigational Drugs 20, no. 3 (February 9, 2011): 423–25. http://dx.doi.org/10.1517/13543784.2011.554823.

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Noel, Sabrina, Bela Z. Schmidt, Jeremy Haaf, and Teresinha Leal. "Cystic fibrosis transmembrane conductance regulator modulators in cystic fibrosis: current perspectives." Clinical Pharmacology: Advances and Applications Volume 8 (September 2016): 127–40. http://dx.doi.org/10.2147/cpaa.s100759.

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MacDonald, Kelvin D., Karen R. McKenzie, and Pamela L. Zeitlin. "Cystic Fibrosis Transmembrane Regulator Protein Mutations." Pediatric Drugs 9, no. 1 (2007): 1–10. http://dx.doi.org/10.2165/00148581-200709010-00001.

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Dawson, David C., and Stephen S. Smith. "Commentary Cystic Fibrosis Transmembrane Conductance Regulator." Journal of General Physiology 110, no. 4 (October 1, 1997): 337–39. http://dx.doi.org/10.1085/jgp.110.4.337.

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Zemanick, Edith T., and Frank J. Accurso. "Cystic Fibrosis Transmembrane Conductance Regulator andPseudomonas." American Journal of Respiratory and Critical Care Medicine 189, no. 7 (April 2014): 763–65. http://dx.doi.org/10.1164/rccm.201402-0209ed.

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Riordan, J. R. "The Cystic Fibrosis Transmembrane Conductance Regulator." Annual Review of Physiology 55, no. 1 (October 1993): 609–30. http://dx.doi.org/10.1146/annurev.ph.55.030193.003141.

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Burgener, Elizabeth B., and Richard B. Moss. "Cystic fibrosis transmembrane conductance regulator modulators." Current Opinion in Pediatrics 30, no. 3 (June 2018): 372–77. http://dx.doi.org/10.1097/mop.0000000000000627.

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Corradi, Valentina, Paola Vergani, and D. Peter Tieleman. "Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)." Journal of Biological Chemistry 290, no. 38 (July 30, 2015): 22891–906. http://dx.doi.org/10.1074/jbc.m115.665125.

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Dissertations / Theses on the topic "Cystic fibrosis transmembrane"

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Demolombe, Sophie. "Cftr : ou cystic fibrosis transmembrane conductance regulator." Paris 11, 1996. http://www.theses.fr/1996PA112463.

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La mucoviscidose, maladie genetique grave la plus frequente dans les populations europeenne et nord-americaine, est caracterisee par un defaut de transport d'ions chlore par les cellules epitheliales. Cette affection, transmise selon le mode autosomique recessif, est liee a la mutation du gene cf codant pour la proteine cftr (cystic fibrosis transmembrane conductance regulator) qui exerce un role de canal chlore regule par l'atp intracellulaire et l'ampc. La mutation la plus frequente (70% des alleles mutes) est une deletion de la phenylalanine en position 508 qui conduit a un defaut d'adressage de la proteine neoformee. Par des techniques d'immunomarquages faisant appel a differents anticorps monoclonaux, nous avons montre que l'anomalie moleculaire caracteristique de la mutation f508 est retrouvee dans la lignee cfpac-1 issue d'un carcinome pancreatique preleve chez un patient homozygote pour cette mutation. Cfpac-1 est une lignee cellulaire couramment utilisee pour les investigations biochimiques, physiologiques et pharmacologiques de l'insuffisance cellulaire responsable de la mucoviscidose. Nous avons developpe une nouvelle methode permettant d'evaluer l'efficacite de la complementation par transfert de gene de l'epithelium respiratoire mucoviscidosique. Le principe de cette methode consiste a detecter les proteines cftr recombinantes correctement adressees dans la membrane apicale a l'aide d'un anticorps dirige contre la premiere boucle extracellulaire et utilise sur des cellules vivantes. Cette methode est suffisamment sensible pour etre utilisee sur un petit nombre de cellules prelevees par simple curetage de la surface epitheliale. La fonction de la proteine cftr ne se limite pas a celle de canal chlore. Par un mecanisme inconnu, cftr exerce un role regulateur d'autres canaux ioniques, chlorures et sodiques epitheliaux. Nous avons mis en evidence la regulation par cftr de canaux potassiques epitheliaux rectifiant dans le sens entrant et dont le controle par la voie de l'ampc depend de la presence d'une proteine cftr fonctionnelle. Ces canaux k+ interviendraient dans le controle du potentiel membranaire et participeraient au maintien d'un gradient electro-chimique indispensable a la vectorisation transepitheliale du chlore
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Tucker, Stephen John. "Studies on the cystic fibrosis transmembrane conductance regulator." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357427.

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Marrs, Kevin L. "The cystic fibrosis transmembrane conductance regulator regulation by HSP-90 /." View the abstract Download the full-text PDF version, 2007. http://etd.utmem.edu/ABSTRACTS/2007-031-Marrs-index.html.

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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2007.
Title from title page screen (viewed on July, 18, 2008). Research advisor: Anjaparavanda Naren, Ph.D. Document formatted into pages (xv, 72 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 66-72).
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Glanville, Michael. "The molecular basis of renal tubular anion secretion." Thesis, University of Newcastle Upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273477.

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Bhura-Bandali, Farah. "The cystic fibrosis transmembrane conductance regulator in essential fatty acid metabolism." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22572.pdf.

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GARCIA-FONKNECHTEN, NORIA. "Etude des transcrits du gene cftr. (cystic fibrosis transmembrane conductance regulator)." Paris 7, 1993. http://www.theses.fr/1993PA077156.

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Le gene cftr (cystic fibrosis transmembrane conductance regulator), constitue de 27 exons repartis sur 250 kb et dont l'alteration est responsable de la mucoviscidose, est essentiellement exprime dans les epitheliums respiratoires et digestifs. Cette expression est indetectable par northern-blot dans des cellules facilement accessibles comme les lymphocytes. Cependant, par la technique d'amplification de l'adnc par nested-pcr, nous avons mis en evidence et quantifie les transcrits cftr dans les lymphoblastes (transcription illegitime). Bien qu'ils soient en tres faible quantite, par cette methodologie nous obtenons du materiel en quantite suffisante pour l'analyse moleculaire de ces transcrits. C'est par cette analyse chez un patient homozygote pour la mutation majoritairement retrouvee dans cette maladie (f508), que nous avons prouve que ces transcrits etaient une source de materiel pathologique. Tres encourages par nos premiers resultats et afin d'etudier la totalite du transcrit cftr, nous avons developpe un protocole permettant d'amplifier l'adnc codant (4,2 kb) en six fragments chevauchants. Utilisant cette strategie nous exposons dans ce travail trois applications de cette methode sur l'arn obtenu a partir des lymphoblastes des patients atteints de mucoviscidose: (1) detection de mutations ponctuelles sur de grands fragments d'adnc, ce qui permet d'explorer plusieurs exons de facon simultanee; (2) mise en evidence de transcrits anormaux resultant d'une mutation d'epissage; (3) detection de transcrits anormaux, s'agissant le plus souvent de la perte d'exons, chez des malades ne presentant aucune mutation d'epissage. Ces transcrits seraient issus d'un epissage aberrant ou alternatif. Des transcrits depourvus des exons 9 ou 12 ont ete egalement detectes chez les sujets normaux. Enfin, pour mieux comprendre ce phenomene d'epissage alternatif ou aberrant nous avons etudie les transcrits depourvus de l'exon 9 dans le pancreas humain normal, l'un des sites d'expression du gene cftr. Cette etude nous a permis la mise en evidence de tels transcrits dans les tissus pancreatiques a differents ages du developpement embryonnaire, ainsi que chez l'adulte
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Qureshi, Emili Alia. "Expression and purification of transmembrane segments 3 and 4 of the cystic fibrosis transmembrane conductance regulator." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0007/MQ29199.pdf.

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Hull, Jeremy. "Mutation analysis and screening in the cystic fibrosis transmembrane conductance regulator gene." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260734.

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Holleran, John. "Fluorescence Platform Development for Detection of Cystic Fibrosis Transmembrane Conductance Regulator Trafficking." Research Showcase @ CMU, 2011. http://repository.cmu.edu/dissertations/97.

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Cystic fibrosis is caused by mutations in the membrane chloride channel, cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation, ΔF508, disrupts protein folding resulting in premature degradation which precludes expression at the cell surface. Therapeutic strategies have been developed to rescue ΔF508 by using small molecules, called correctors, which promote folding and trafficking to the surface. Currently, the discovery and evaluation of these correctors requires indirect functional measurements or time intensive biochemical methods. In order to facilitate faster analysis of corrector compounds and provide a screening assay that directly monitors rescue of ΔF508 trafficking, we developed a rapid fluorescence detection platform using fluorogen activating proteins (FAPs) capable of labeling of CFTR at the cell surface. We created two chimeric reporter constructs by fusing the FAP to the N-terminus, or by insertion of the FAP into the fourth extracellular loop. We expressed these constructs in HEK293 cells and verified that the ion transport function, biochemical properties and cellular localization reproduced the native behavior of CFTR. Under normal conditions, CFTR ΔF508 is absent from the surface, however incubation in the presence of correctors restored trafficking to the plasma membrane that was robustly detected by FAP fluorescence. Using this approach we have characterized the efficacy of two new corrector compounds C548, C951 and the well-studied reference corrector, C4. The most potent corrector identified was C951 which performed 2 fold better than the previously described, C4 corrector. Other studies have shown that combinations of correctors exhibit an additive or synergistic effect, therefore, we tested combinations of correctors using FAP-CFTR constructs and found they had a synergistic effect on the rescue of ΔF508, improving the density of protein at the cell surface 4 fold greater than C4 alone. These results correlated closely with functional data obtained from polarized human bronchial epithelia that endogenously express ΔF508, suggesting that the FAP tagged CFTR reporters represent a physiologically faithful model of corrector rescue.
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Al, Salmani Majid Khamis Ali. "Functional studies of rare mutations in the cystic fibrosis transmembrane conductance regulator." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.738550.

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Books on the topic "Cystic fibrosis transmembrane"

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Kirk, Kevin L. The cystic fibrosis transmembrane conductance regulator. Georgetown, Tex: Landes Bioscience / Eurekah.com, 2003.

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Kirk, Kevin L. The cystic fibrosis transmembrane conductance regulator. Georgetown, TX: Landes Bioscience : Eurekah.com, 2004.

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Emili, Alia Qureshi. Expression and purification of transmembrane segments 3 and 4 of the cystic fibrosis transmembrane conductance regulator. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Seibert, Fabian S. Structure-function relationships of the cytoplasmic domains of the cystic fibrosis transmembrane conductance regulator. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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Wong, Melanie Hoi-Lee. The role of the C-terminus in the cellular physiology of cystic fibrosis transmembrane-conductance regulator (CTFR). Ottawa: National Library of Canada, 2000.

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Grondin, Ronald Thomas. Expression, purification, refolding, and ATP binding of the first nucleotide binding domain of the cystic fibrosis transmembrane conductance regulator. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Li, Xiaobin. Characterization of multiple copies of a DNA segment containing cystic fibrosis transmembrane conductance regulator gene exon 9 in the human genome. Ottawa: National Library of Canada, 1999.

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Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Cystic fibrosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0021.

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Gastrointestinal manifestations 156Management of gastrointestinal symptoms in children with CF 158Nutrition in CF 158Nutritional management 159Vitamins 160The incidence of cystic fibrosis (CF) is around 1 in 2500. Cases are diagnosed as a consequence of population screening or high-risk screening, or following presentation with clinical symptoms typical of the disorder. The basic defect is in the CFTR (cystic fibrosis transmembrane conductance regulator) protein which codes for a cyclic adenosine monophosphate-regulated chloride transporter in epithelial cells of exocrine organs. This is involved in salt and water balance across epithelial surfaces. The gene is on chromosome 7. There are multiple known mutations, the most common being ...
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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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Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Cystic fibrosis-associated liver disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0022.

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Pathophysiology 162Clinical features 162Diagnosis 163Management 164Cystic fibrosis (CF) is an autosomal recessive disease resulting from mutations in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) (see Chapter 21). CFTR functions as a transmembrane chloride channel in the apical membrane of most secretory epithelia and the disease thus affects lungs, pancreas, exocrine glands, gut, and liver. In CF-associated liver disease the biliary tract is most commonly involved in a spectrum from asymptomatic to biliary cirrhosis. The liver disease runs from mild and subclinical to severe cirrhosis and portal hypertension. Clinical disease is seen in 4–6% of cases, but there are biochemical abnormalities in 20–50%. At autopsy, fibrosis is present in 20% and steatosis in 50%....
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Book chapters on the topic "Cystic fibrosis transmembrane"

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Stratford, Fiona L. L., and Christine E. Bear. "Structure of the Cystic Fibrosis Transmembrane Conductance Regulator." In Cystic Fibrosis in the 21st Century, 29–37. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000088471.

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Bridges, Robert J., and Neil A. Bradbury. "Cystic Fibrosis, Cystic Fibrosis Transmembrane Conductance Regulator and Drugs: Insights from Cellular Trafficking." In Targeting Trafficking in Drug Development, 385–425. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_103.

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Solomon, George M., and Steven M. Rowe. "Functional Evaluation of Cystic Fibrosis Transmembrane Conductance Regulator." In Diagnostic Tests in Pediatric Pulmonology, 73–91. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1801-0_5.

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Anderson, Matthew P., Devra P. Rich, Richard J. Gregory, Seng Cheng, Alan E. Smith, and Michael J. Welsh. "Function and Regulation of the Cystic Fibrosis Transmembrane Conductance Regulator." In Adenine Nucleotides in Cellular Energy Transfer and Signal Transduction, 399–413. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7315-4_36.

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Al Salmani, Majid K., Elvira Sondo, Corina Balut, David N. Sheppard, Ashvani K. Singh, and Nicoletta Pedemonte. "Molecular Physiology and Pharmacology of the Cystic Fibrosis Transmembrane Conductance Regulator." In Studies of Epithelial Transporters and Ion Channels, 605–70. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-55454-5_16.

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Kunzelmann, K. "The cystic fibrosis transmembrane conductance regulator and its function in epithelial transport." In Reviews of Physiology, Biochemistry and Pharmacology, Volume 137, 1–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/3-540-65362-7_4.

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Schwarz, Martin, Claire Summers, Lesley Heptinstall, Clive Newton, Alexander Markham, and Maurice Super. "A Deletion Mutation of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Locus: DeltaI507." In Advances in Experimental Medicine and Biology, 393–98. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5934-0_48.

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Linsdell, Paul. "Structural Changes Fundamental to Gating of the Cystic Fibrosis Transmembrane Conductance Regulator Anion Channel Pore." In Advances in Experimental Medicine and Biology, 13–32. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/5584_2016_33.

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Partridge, Anthony W., Roman A. Melnyk, and Charles M. Deber. "Covalent and Non-Covalent Oligomerization of the Transmembrane α-Helix 4 from the Cystic Fibrosis Conductance Regulator." In Peptides: The Wave of the Future, 820–21. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_383.

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Patrizio, Pasquale, and Ricardo H. Asch. "Congenital Absence of the Vas Deferens and the Cystic Fibrosis Transmembrane Conductance Regulator Gene: Evidence for a Common Genetic Background." In Function of Somatic Cells in the Testis, 430–37. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2638-3_28.

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Conference papers on the topic "Cystic fibrosis transmembrane"

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Wilhelm, Andrew M., Mark Dransfield, Navnit Mehta, and Steve Rowe. "Cystic Fibrosis Transmembrane Conductance Regulator Function In Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3021.

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Tabeling, Christoph, Hanpo Yu, Liming Wang, Hannes Ranke, Neil M. Goldenberg, Diana Zabini, Elena Noe, et al. "Cystic fibrosis transmembrane conductance regulator and sphingolipids regulate hypoxic pulmonary vasoconstriction." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4905.

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Aridgides, D., D. Mellinger, J. Dessaint, G. Atkins, J. L. Carroll, and A. Ashare. "Cystic Fibrosis Transmembrane Conductance Regulator Modulators Enhance Phagocytosis by Smoker Macrophages." 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.a1224.

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Williams, Kurt, Heather DeFeijter-Rupp, and Kevin Kroner. "Regional Distribution Of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) In The Caprine Respiratory Tract." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4223.

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Wilhelm, Andrew M., Mark T. Dransfield, Cliff Courville, L. P. Tang, S. Shastry, Heather Young, Ginger Reeves, G. Sabbatini, and Steven M. Rowe. "Reduced Cystic Fibrosis Transmembrane Conductance Regulator Function In Smoke Induced Chronic Obstructive Pulmonary Disease." 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.a2920.

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Raju, Sammeta V., Gina Sabbatini, Peter A. Sloane, Li Ping Tang, Frank Accurso, Mark T. Dransfield, and Steven M. Rowe. "Cigarette Smoke Induces Systemic Defects In Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Ion Transport." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3522.

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Worthington, E., and J. L. Goralski. "A Unique Phenotype of a Rare Cystic Fibrosis Transmembrane Regulator Gene Mutation: C.935_937deltct (p.Phe312del)." 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.a3159.

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Choi, E., GE Lee, HM Cho, YJ Kim, SJ Kwon, MJ Na, and JW Son. "Quantitative Evaluation of Methylation for Cystic Fibrosis Transmembrane Regulator Gene in Non-Small Cell Lung Cancer." 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.a5014.

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Polineni, Deepika, Ray Coakley, and Michael R. Knowles. "Distal Intestinal Obstructive Syndrome (DIOS) Complicating Severe Cystic Fibrosis (CF) Lung Disease In A Patient Carrying A "Pancreatic Sufficient" Mutation In Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5410.

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Kataria, N., I. Randhawa, E. Nussbaum, T. Morphew, K. Singh, T. W. Chin, and C. Shahriary. "Clinical Outcomes in Patients with Cystic Fibrosis Transmembrane Conductance Regulator-Related Metabolic Syndrome at a Single Center." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1905.

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