Antisense oligodeoxynucleotides to the cystic fibrosis transmembrane conductance regulator inhibit cAMP-activated but not calcium-activated chloride currents.
Identifieur interne : 002816 ( PubMed/Checkpoint ); précédent : 002815; suivant : 002817Antisense oligodeoxynucleotides to the cystic fibrosis transmembrane conductance regulator inhibit cAMP-activated but not calcium-activated chloride currents.
Auteurs : J A Wagner [États-Unis] ; T V Mcdonald ; P T Nghiem ; A W Lowe ; H. Schulman ; D C Gruenert ; L. Stryer ; P. GardnerSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 1992.
Descripteurs français
- KwdFr :
- AMP cyclique (analogues et dérivés), AMP cyclique (métabolisme), AMP cyclique (pharmacologie), ARN messager (génétique), ARN messager (métabolisme), Calcium (pharmacologie), Canaux chlorure, Canaux ioniques (), Données de séquences moléculaires, Humains, Ionomycine (pharmacologie), Lignée cellulaire, Modèles biologiques, Mucoviscidose (génétique), Oligonucléotides antisens (pharmacologie), Phosphorylation, Protéine CFTR, Protéines membranaires (), Protéines membranaires (génétique), Protéines membranaires (physiologie), Séquence nucléotidique, Thionucléotides (pharmacologie).
- MESH :
- analogues et dérivés : AMP cyclique.
- génétique : ARN messager, Mucoviscidose, Protéines membranaires.
- métabolisme : AMP cyclique, ARN messager.
- pharmacologie : AMP cyclique, Calcium, Ionomycine, Oligonucléotides antisens, Thionucléotides.
- physiologie : Protéines membranaires.
- Canaux chlorure, Canaux ioniques, Données de séquences moléculaires, Humains, Lignée cellulaire, Modèles biologiques, Phosphorylation, Protéine CFTR, Protéines membranaires, Séquence nucléotidique.
English descriptors
- KwdEn :
- Base Sequence, Calcium (pharmacology), Cell Line, Chloride Channels, Cyclic AMP (analogs & derivatives), Cyclic AMP (metabolism), Cyclic AMP (pharmacology), Cystic Fibrosis (genetics), Cystic Fibrosis Transmembrane Conductance Regulator, Humans, Ion Channels (drug effects), Ionomycin (pharmacology), Membrane Proteins (drug effects), Membrane Proteins (genetics), Membrane Proteins (physiology), Models, Biological, Molecular Sequence Data, Oligonucleotides, Antisense (pharmacology), Phosphorylation, RNA, Messenger (genetics), RNA, Messenger (metabolism), Thionucleotides (pharmacology).
- MESH :
- chemical , analogs & derivatives : Cyclic AMP.
- chemical , drug effects : Ion Channels, Membrane Proteins.
- chemical , genetics : Membrane Proteins, RNA, Messenger.
- chemical , metabolism : Cyclic AMP, RNA, Messenger.
- chemical , pharmacology : Calcium, Cyclic AMP, Ionomycin, Oligonucleotides, Antisense, Thionucleotides.
- genetics : Cystic Fibrosis.
- chemical , physiology : Membrane Proteins.
- Base Sequence, Cell Line, Chloride Channels, Cystic Fibrosis Transmembrane Conductance Regulator, Humans, Models, Biological, Molecular Sequence Data, Phosphorylation.
Abstract
Phosphorylation of the cystic fibrosis transmembrane conductance regulator (CFTR) by cAMP-dependent protein kinase leads to chloride flux in epithelial cells. Is CFTR also required for the calcium-dependent activation of chloride channels? We used antisense oligodeoxynucleotides to CFTR to reduce the expression of CFTR in colonic and tracheal epithelial cells. The antisense oligomers were a pair of adjacent 18-mers complementary to nucleotides 1-18 and 19-36 of CFTR mRNA. Sense and misantisense oligomers served as controls. A 48-h antisense treatment reduced the expression of CFTR protein as assayed by immunoprecipitation and autoradiography to 26% of the level in sense-treated T84 cells. Whole-cell patch clamp revealed that a 48-h antisense treatment of T84 and 56FHTE-8o- fetal tracheal epithelial cells reduced the cAMP-activated chloride current to approximately 10% of that in sense-treated cells. The half-life of functional CFTR is less than 24 h in these cells. In contrast, the calcium-activated chloride current was not affected by antisense treatment. Hence, the cAMP and calcium pathways are separate. CFTR is required for the cAMP pathway but not for the calcium pathway.
DOI: 10.1073/pnas.89.15.6785
PubMed: 1379720
Affiliations:
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Is CFTR also required for the calcium-dependent activation of chloride channels? We used antisense oligodeoxynucleotides to CFTR to reduce the expression of CFTR in colonic and tracheal epithelial cells. The antisense oligomers were a pair of adjacent 18-mers complementary to nucleotides 1-18 and 19-36 of CFTR mRNA. Sense and misantisense oligomers served as controls. A 48-h antisense treatment reduced the expression of CFTR protein as assayed by immunoprecipitation and autoradiography to 26% of the level in sense-treated T84 cells. Whole-cell patch clamp revealed that a 48-h antisense treatment of T84 and 56FHTE-8o- fetal tracheal epithelial cells reduced the cAMP-activated chloride current to approximately 10% of that in sense-treated cells. The half-life of functional CFTR is less than 24 h in these cells. In contrast, the calcium-activated chloride current was not affected by antisense treatment. Hence, the cAMP and calcium pathways are separate. CFTR is required for the cAMP pathway but not for the calcium pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1379720</PMID><DateCompleted><Year>1992</Year><Month>09</Month><Day>04</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0027-8424</ISSN><JournalIssue CitedMedium="Print"><Volume>89</Volume><Issue>15</Issue><PubDate><Year>1992</Year><Month>Aug</Month><Day>01</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>Antisense oligodeoxynucleotides to the cystic fibrosis transmembrane conductance regulator inhibit cAMP-activated but not calcium-activated chloride currents.</ArticleTitle><Pagination><MedlinePgn>6785-9</MedlinePgn></Pagination><Abstract><AbstractText>Phosphorylation of the cystic fibrosis transmembrane conductance regulator (CFTR) by cAMP-dependent protein kinase leads to chloride flux in epithelial cells. Is CFTR also required for the calcium-dependent activation of chloride channels? We used antisense oligodeoxynucleotides to CFTR to reduce the expression of CFTR in colonic and tracheal epithelial cells. The antisense oligomers were a pair of adjacent 18-mers complementary to nucleotides 1-18 and 19-36 of CFTR mRNA. Sense and misantisense oligomers served as controls. A 48-h antisense treatment reduced the expression of CFTR protein as assayed by immunoprecipitation and autoradiography to 26% of the level in sense-treated T84 cells. Whole-cell patch clamp revealed that a 48-h antisense treatment of T84 and 56FHTE-8o- fetal tracheal epithelial cells reduced the cAMP-activated chloride current to approximately 10% of that in sense-treated cells. The half-life of functional CFTR is less than 24 h in these cells. In contrast, the calcium-activated chloride current was not affected by antisense treatment. Hence, the cAMP and calcium pathways are separate. CFTR is required for the cAMP pathway but not for the calcium pathway.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wagner</LastName><ForeName>J A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Department of Medicine, Falk Cardiovascular Research Center, Stanford University School of Medicine, CA 94305.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McDonald</LastName><ForeName>T V</ForeName><Initials>TV</Initials></Author><Author ValidYN="Y"><LastName>Nghiem</LastName><ForeName>P T</ForeName><Initials>PT</Initials></Author><Author ValidYN="Y"><LastName>Lowe</LastName><ForeName>A W</ForeName><Initials>AW</Initials></Author><Author ValidYN="Y"><LastName>Schulman</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Gruenert</LastName><ForeName>D C</ForeName><Initials>DC</Initials></Author><Author ValidYN="Y"><LastName>Stryer</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Gardner</LastName><ForeName>P</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505032">CFTR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018118">Chloride Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007473">Ion Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016376">Oligonucleotides, Antisense</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013873">Thionucleotides</NameOfSubstance></Chemical><Chemical><RegistryNumber>126880-72-6</RegistryNumber><NameOfSubstance UI="D019005">Cystic Fibrosis Transmembrane Conductance Regulator</NameOfSubstance></Chemical><Chemical><RegistryNumber>41941-66-6</RegistryNumber><NameOfSubstance UI="C015929">8-((4-chlorophenyl)thio)cyclic-3',5'-AMP</NameOfSubstance></Chemical><Chemical><RegistryNumber>56092-81-0</RegistryNumber><NameOfSubstance UI="D015759">Ionomycin</NameOfSubstance></Chemical><Chemical><RegistryNumber>E0399OZS9N</RegistryNumber><NameOfSubstance UI="D000242">Cyclic AMP</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018118" MajorTopicYN="N">Chloride Channels</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000242" MajorTopicYN="N">Cyclic AMP</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003550" MajorTopicYN="N">Cystic Fibrosis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019005" MajorTopicYN="N">Cystic Fibrosis Transmembrane Conductance Regulator</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007473" MajorTopicYN="N">Ion Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015759" MajorTopicYN="N">Ionomycin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016376" MajorTopicYN="N">Oligonucleotides, Antisense</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName 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Gardner</name><name sortKey="Gruenert, D C" sort="Gruenert, D C" uniqKey="Gruenert D" first="D C" last="Gruenert">D C Gruenert</name><name sortKey="Lowe, A W" sort="Lowe, A W" uniqKey="Lowe A" first="A W" last="Lowe">A W Lowe</name><name sortKey="Mcdonald, T V" sort="Mcdonald, T V" uniqKey="Mcdonald T" first="T V" last="Mcdonald">T V Mcdonald</name><name sortKey="Nghiem, P T" sort="Nghiem, P T" uniqKey="Nghiem P" first="P T" last="Nghiem">P T Nghiem</name><name sortKey="Schulman, H" sort="Schulman, H" uniqKey="Schulman H" first="H" last="Schulman">H. Schulman</name><name sortKey="Stryer, L" sort="Stryer, L" uniqKey="Stryer L" first="L" last="Stryer">L. Stryer</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Wagner, J A" sort="Wagner, J A" uniqKey="Wagner J" first="J A" last="Wagner">J A Wagner</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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