Source:http://linkedlifedata.com/resource/pubmed/id/18773956
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
2008-9-23
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| pubmed:abstractText |
Cystic fibrosis (CF) is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. In CF, the most common mutant DeltaF508-CFTR is misfolded, is retained in the ER and is rapidly degraded. If conditions could allow DeltaF508-CFTR to reach and to stabilize in the plasma membrane, it could partially correct the CF defect. We have previously shown that annexin V (anxA5) binds to both the normal CFTR and the DeltaF508-CFTR in a Ca(2+)-dependent manner and that it regulates the chloride channel function of Wt-CFTR through its membrane integration. Our aim was to extend this finding to the DeltaF508-CFTR. Because some studies show that thapsigargin (Tg) increases the DeltaF508-CFTR apical expression and induces an increased [Ca(2+)](i) and because anxA5 relocates and binds to the plasma membrane in the presence of Ca(2+), we hypothesized that the Tg effect upon DeltaF508-CFTR function could involve anxA5. Our results show that raised anxA5 expression induces an augmented function of DeltaF508-CFTR due to its increased membrane localization. Furthermore, we show that the Tg effect involves anxA5. Therefore, we suggest that anxA5 is a potential therapeutic target in CF.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Annexin A5,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cystic Fibrosis Transmembrane...,
http://linkedlifedata.com/resource/pubmed/chemical/Thapsigargin,
http://linkedlifedata.com/resource/pubmed/chemical/cystic fibrosis transmembrane...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0006-3002
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
1782
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
605-14
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| pubmed:meshHeading |
pubmed-meshheading:18773956-Annexin A5,
pubmed-meshheading:18773956-Blotting, Western,
pubmed-meshheading:18773956-Calcium,
pubmed-meshheading:18773956-Cell Line, Tumor,
pubmed-meshheading:18773956-Cell Membrane,
pubmed-meshheading:18773956-Cyclic AMP,
pubmed-meshheading:18773956-Cystic Fibrosis Transmembrane Conductance Regulator,
pubmed-meshheading:18773956-Cytoplasm,
pubmed-meshheading:18773956-Epithelial Cells,
pubmed-meshheading:18773956-Humans,
pubmed-meshheading:18773956-Immunoprecipitation,
pubmed-meshheading:18773956-Ion Channel Gating,
pubmed-meshheading:18773956-Membrane Potentials,
pubmed-meshheading:18773956-Mutation,
pubmed-meshheading:18773956-Patch-Clamp Techniques,
pubmed-meshheading:18773956-Protein Binding,
pubmed-meshheading:18773956-RNA Interference,
pubmed-meshheading:18773956-Thapsigargin,
pubmed-meshheading:18773956-Transfection
|
| pubmed:year |
2008
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| pubmed:articleTitle |
Annexin A5 increases the cell surface expression and the chloride channel function of the DeltaF508-cystic fibrosis transmembrane regulator.
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| pubmed:affiliation |
Inserm, U613, Brest, F-29200, France.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|