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pubmed-article:8944727pubmed:abstractTextChloride channels supply critical functions in epithelial cells throughout the body. Although function of the volume- and voltage-gated C1C-2 is uncertain, its wide tissue distribution of mRNA suggests C1C-2 has important housekeeping functions. This study's objective was to identify the extent of not only C1C-2 mRNA expression but also protein expression as a measure of the capacity for C1C-2 chloride secretion in epithelial tissues. Using quantitative ribonuclease protection assay, we found that C1C-2 mRNA transcripts were abundant in fetal and postnatal brain, fetal kidney, liver, intestine, and lung. In contrast to brain, C1C-2 mRNA transcripts were downregulated during late gestation in lung, kidney, and intestine. The lung expressed the least C1C-2 mRNA. Immunoblotting demonstrated similar tissue- and gestation-dependent variations in C1C-2 protein expression. To determine if there is a correlation between the sites of C1C-2 protein expression and cystic fibrosis transmembrane conductance regulator (CFTR), another epithelial chloride channel, a polyclonal COOH-terminal C1C-2 antibody and an anti-R domain CFTR anti-body were used. C1C-2 and CFTR were expressed in different sites in lung and kidney.lld:pubmed
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pubmed-article:8944727pubmed:articleTitleGestational and tissue-specific regulation of C1C-2 chloride channel expression.lld:pubmed
pubmed-article:8944727pubmed:affiliationEudowood Division of Respiratory Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287, USA.lld:pubmed
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pubmed-article:8944727pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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