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http://purl.uniprot.org/citations/16822950http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16822950http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16822950http://www.w3.org/2000/01/rdf-schema#comment"The mechanisms underlying regulatory interactions of the cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial Na(+) channel (ENaC) in Xenopus oocytes are controversial. CFTR's first nucleotide binding domain (NBD-1) may be important in these interactions, because mutations within NBD-1 impair these functional interactions. We hypothesized that an abnormal CFTR containing a non-NBD-1 mutation and able to transport chloride would retain regulatory interactions with murine ENaC (mENaC). We tested this hypothesis for I148T-CFTR, where the mutation is located in CFTR's first intracellular loop. I148T-CFTR has been associated with a severe CF phenotype, perhaps because of defects in its regulation of bicarbonate transport, but it transports chloride similarly to wild-type CFTR in model systems (Choi JY, Muallem D, Kiselyov K, Lee MG, Thomas PJ, Muallem S. Nature 410: 94-97, 2001). cRNAs encoding alphabetagamma-mENaC and I148T-CFTR were injected separately or together into Xenopus oocytes. mENaC and CFTR functional expression were assessed by two-electrode voltage clamp. mENaC whole oocyte expression was determined by immunoblotting, and surface expression was quantitated by surface biotinylation. Injection of I148T-CFTR cRNA alone yielded high levels of CFTR functional expression. In coinjected oocytes, mENaC functional and surface expression was not altered by activation of I148T-CFTR with forskolin/ IBMX. Furthermore, the CFTR potentiator genistein both enhanced functional expression of I148T-CFTR and restored regulation of mENaC surface expression by activated I148T-CFTR. These data suggest that the ability to transport chloride is not a critical determinant of regulation of mENaC by activated CFTR in Xenopus oocytes and provide further evidence that I148T-CFTR is dysfunctional despite maintaining the ability to transport chloride."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.org/dc/terms/identifier"doi:10.1152/ajpcell.00088.2006"xsd:string
http://purl.uniprot.org/citations/16822950http://purl.org/dc/terms/identifier"doi:10.1152/ajpcell.00088.2006"xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/author"Yan W."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/author"Yan W."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/author"Rubenstein R.C."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/author"Rubenstein R.C."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/author"Suaud L."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/author"Suaud L."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/name"Am. J. Physiol."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/name"Am. J. Physiol."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/pages"C603-C611"xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/pages"C603-C611"xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/title"Abnormal regulatory interactions of I148T-CFTR and the epithelial Na+ channel in Xenopus oocytes."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/title"Abnormal regulatory interactions of I148T-CFTR and the epithelial Na+ channel in Xenopus oocytes."xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/volume"292"xsd:string
http://purl.uniprot.org/citations/16822950http://purl.uniprot.org/core/volume"292"xsd:string
http://purl.uniprot.org/citations/16822950http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16822950
http://purl.uniprot.org/citations/16822950http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16822950
http://purl.uniprot.org/citations/16822950http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16822950
http://purl.uniprot.org/citations/16822950http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16822950