Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-6-21
pubmed:abstractText
Cystic fibrosis is a common lethal heritable disorder, caused by a defect in a chloride channel protein, namely CFTR. After the identification of the gene and its product by positional cloning (on chromosome 7), CFTR has been characterized as a low conductance (8-10 pSiemens) linear chloride channel, which appears to regulate other apical transport proteins. Two therapeutic options are reviewed: gene transfection and drug therapy. So far, clinical studies have shown that gene transfection cannot effectively restore CFTR function. Simultaneously, several drugs including genistein, phenylimidazothiazoles and gentamicin have been found to activate mutant CFTR, thus, being suitable for single or combined (with gene transfection) treatment.
pubmed:language
spa
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0212-7199
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
92-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
[From the laboratory to the clinic: CFTR and the therapeutic options for cystic fibrosis].
pubmed:affiliation
Servicio de Cirugía I, Hospital Clínico San Carlos, Madrid. j.mayol@mad.servicom.es
pubmed:publicationType
Journal Article, English Abstract, Review, Research Support, Non-U.S. Gov't