| pubmed-article:7512555 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7512555 | lifeskim:mentions | umls-concept:C0010674 | lld:lifeskim |
| pubmed-article:7512555 | lifeskim:mentions | umls-concept:C0055363 | lld:lifeskim |
| pubmed-article:7512555 | lifeskim:mentions | umls-concept:C0105592 | lld:lifeskim |
| pubmed-article:7512555 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:7512555 | pubmed:dateCreated | 1994-5-19 | lld:pubmed |
| pubmed-article:7512555 | pubmed:abstractText | Cystic fibrosis is a major inherited disorder involving abnormalities of fluid and electrolyte transport in a number of different organs. Epithelial cells of cystic fibrosis patients have a decreased capacity to secrete chloride in response to cAMP-mobilizing agents because of the mutation of a single gene. The gene product, the cystic fibrosis transmembrane conductance regulator or CFTR, is a chloride channel. The most frequent mutation is a deletion of phenylalanine in position 508 (delta F508-CFTR) that reduces both the expression of the CFTR protein at the cell surface, and the activity of the Cl- channel. This work presents the properties of NS004, a substituted benzimidazolone, which is the first activator of normal and mutant CFTR-associated chloride channels to be described. NS004 activated CFTR and delta F508-CFTR Cl- channels expressed in Xenopus oocytes, and increased 125I efflux (via the Cl- channel) from Vero cells expressing CFTR and delta F508-CFTR. Application of NS004 to the external side of outside-out patches excised from these CFTR- and delta F508-CFTR-expressing cells induced a marked and reversible increase in channel activity. | lld:pubmed |
| pubmed-article:7512555 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7512555 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7512555 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7512555 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7512555 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:7512555 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:7512555 | pubmed:author | pubmed-author:LazdunskiMM | lld:pubmed |
| pubmed-article:7512555 | pubmed:author | pubmed-author:GribkoffV KVK | lld:pubmed |
| pubmed-article:7512555 | pubmed:author | pubmed-author:MeanwellN ANA | lld:pubmed |
| pubmed-article:7512555 | pubmed:author | pubmed-author:DworetzkyS... | lld:pubmed |
| pubmed-article:7512555 | pubmed:author | pubmed-author:ChampignyGG | lld:pubmed |
| pubmed-article:7512555 | pubmed:author | pubmed-author:BarbryPP | lld:pubmed |
| pubmed-article:7512555 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7512555 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:7512555 | pubmed:volume | 269 | lld:pubmed |
| pubmed-article:7512555 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7512555 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7512555 | pubmed:pagination | 10983-6 | lld:pubmed |
| pubmed-article:7512555 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:7512555 | pubmed:meshHeading | pubmed-meshheading:7512555-... | lld:pubmed |
| pubmed-article:7512555 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7512555 | pubmed:articleTitle | The substituted benzimidazolone NS004 is an opener of the cystic fibrosis chloride channel. | lld:pubmed |
| pubmed-article:7512555 | pubmed:affiliation | Department of Central Nervous System Biophysics and Molecular Biology, Bristol-Myers Squibb Pharmaceutical Research Institute, Wallingford, Connecticut 06492. | lld:pubmed |
| pubmed-article:7512555 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7512555 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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