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Article: cAMP-inducible chloride conductance in mouse fibroblast lines stably expressing the human cystic fibrosis transmembrane conductance regulator
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TitlecAMP-inducible chloride conductance in mouse fibroblast lines stably expressing the human cystic fibrosis transmembrane conductance regulator
 
AuthorsRommens, JM1
Dho, S1
Bear, CE1
Kartner, N1
Kennedy, D1
Riordan, JR1
Tsui, LC1
Foskett, JK1
 
KeywordscAMP regulation
chloride channel
full-length cDNA
 
Issue Date1991
 
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
 
CitationProceedings Of The National Academy Of Sciences Of The United States Of America, 1991, v. 88 n. 17, p. 7500-7504 [How to Cite?]
 
AbstractA cAMP-inducible chloride permeability has been detected in mouse fibroblast (L cell) lines upon stable integration of a full-length cDNA encoding the human cystic fibrosis transmembrane conductance regulator (CFTR). As indicated by a Cl--indicator dye, the Cl- permeability of the plasma membrane increases by 10- to 30-fold within 2 min after treatment of the cells with forskolin, an activator of adenylyl cyclase. The properties of the conductance are similar to those described in secretory epithelial cells; the whole-cell current-voltage relationship is linear and there is no evidence of voltage-dependent inactivation or activation. In contrast, this cAMP-dependent Cl- flux is undetectable in the untransfected cells or cells harboring defective cDNA constructs, including one with a phenylalanine deletion at amino acid position 508 (ΔF508), the most common mutation causing cystic fibrosis. These observations are consistent with the hypothesis that the CFTR is a cAMP-dependent Cl- channel. The availability of a heterologous (nonepithelial) cell type expressing the CFTR offers an excellent system to understand the basic mechanisms underlying this CFTR-associated ion permeability and to study the structure and function of the CFTR.
 
ISSN0027-8424
2012 Impact Factor: 9.737
2012 SCImago Journal Rankings: 5.473
 
PubMed Central IDPMC52328
 
ISI Accession Number IDWOS:A1991GC99200010
 
DC FieldValue
dc.contributor.authorRommens, JM
 
dc.contributor.authorDho, S
 
dc.contributor.authorBear, CE
 
dc.contributor.authorKartner, N
 
dc.contributor.authorKennedy, D
 
dc.contributor.authorRiordan, JR
 
dc.contributor.authorTsui, LC
 
dc.contributor.authorFoskett, JK
 
dc.date.accessioned2007-09-12T03:49:48Z
 
dc.date.available2007-09-12T03:49:48Z
 
dc.date.issued1991
 
dc.description.abstractA cAMP-inducible chloride permeability has been detected in mouse fibroblast (L cell) lines upon stable integration of a full-length cDNA encoding the human cystic fibrosis transmembrane conductance regulator (CFTR). As indicated by a Cl--indicator dye, the Cl- permeability of the plasma membrane increases by 10- to 30-fold within 2 min after treatment of the cells with forskolin, an activator of adenylyl cyclase. The properties of the conductance are similar to those described in secretory epithelial cells; the whole-cell current-voltage relationship is linear and there is no evidence of voltage-dependent inactivation or activation. In contrast, this cAMP-dependent Cl- flux is undetectable in the untransfected cells or cells harboring defective cDNA constructs, including one with a phenylalanine deletion at amino acid position 508 (ΔF508), the most common mutation causing cystic fibrosis. These observations are consistent with the hypothesis that the CFTR is a cAMP-dependent Cl- channel. The availability of a heterologous (nonepithelial) cell type expressing the CFTR offers an excellent system to understand the basic mechanisms underlying this CFTR-associated ion permeability and to study the structure and function of the CFTR.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 1991, v. 88 n. 17, p. 7500-7504 [How to Cite?]
 
dc.identifier.epage7504
 
dc.identifier.isiWOS:A1991GC99200010
 
dc.identifier.issn0027-8424
2012 Impact Factor: 9.737
2012 SCImago Journal Rankings: 5.473
 
dc.identifier.issue17
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC52328
 
dc.identifier.pmid1715567
 
dc.identifier.scopuseid_2-s2.0-0025807911
 
dc.identifier.spage7500
 
dc.identifier.urihttp://hdl.handle.net/10722/44246
 
dc.identifier.volume88
 
dc.languageeng
 
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America
 
dc.subject.meshChlorides - metabolism
 
dc.subject.meshFull-length cdna
 
dc.subject.meshChloride channel
 
dc.subject.meshCamp regulation
 
dc.subject.meshCystic fibrosis - genetics - physiopathology
 
dc.subjectcAMP regulation
 
dc.subjectchloride channel
 
dc.subjectfull-length cDNA
 
dc.titlecAMP-inducible chloride conductance in mouse fibroblast lines stably expressing the human cystic fibrosis transmembrane conductance regulator
 
dc.typeArticle
 
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<contributor.author>Dho, S</contributor.author>
<contributor.author>Bear, CE</contributor.author>
<contributor.author>Kartner, N</contributor.author>
<contributor.author>Kennedy, D</contributor.author>
<contributor.author>Riordan, JR</contributor.author>
<contributor.author>Tsui, LC</contributor.author>
<contributor.author>Foskett, JK</contributor.author>
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<description.abstract>A cAMP-inducible chloride permeability has been detected in mouse fibroblast (L cell) lines upon stable integration of a full-length cDNA encoding the human cystic fibrosis transmembrane conductance regulator (CFTR). As indicated by a Cl--indicator dye, the Cl- permeability of the plasma membrane increases by 10- to 30-fold within 2 min after treatment of the cells with forskolin, an activator of adenylyl cyclase. The properties of the conductance are similar to those described in secretory epithelial cells; the whole-cell current-voltage relationship is linear and there is no evidence of voltage-dependent inactivation or activation. In contrast, this cAMP-dependent Cl- flux is undetectable in the untransfected cells or cells harboring defective cDNA constructs, including one with a phenylalanine deletion at amino acid position 508 (&#916;F508), the most common mutation causing cystic fibrosis. These observations are consistent with the hypothesis that the CFTR is a cAMP-dependent Cl- channel. The availability of a heterologous (nonepithelial) cell type expressing the CFTR offers an excellent system to understand the basic mechanisms underlying this CFTR-associated ion permeability and to study the structure and function of the CFTR.</description.abstract>
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Author Affiliations
  1. Hospital for Sick Children University of Toronto