CFTR activity and mitochondrial function
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چکیده
منابع مشابه
CFTR activity and mitochondrial function☆
Cystic Fibrosis (CF) is a frequent and lethal autosomal recessive disease, caused by mutations in the gene encoding the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). Before the discovery of the CFTR gene, several hypotheses attempted to explain the etiology of this disease, including the possible role of a chloride channel, diverse alterations in mitochondrial functions, the overe...
متن کاملIntracellular CFTR: localization and function.
Intracellular CFTR: Localization and Function. Physiol. Rev. 79, Suppl.: S175-S191, 1999. - There is considerable evidence that CFTR can function as a chloride-selective anion channel. Moreover, this function has been localized to the apical membrane of chloride secretory epithelial cells. However, because cystic fibrosis transmembrane conductance regulator (CFTR) is an integral membrane protei...
متن کاملThe Mitochondrial Complex I Activity Is Reduced in Cells with Impaired Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Function
Cystic fibrosis (CF) is a frequent and lethal autosomal recessive disease. It results from different possible mutations in the CFTR gene, which encodes the CFTR chloride channel. We have previously studied the differential expression of genes in CF and CF corrected cell lines, and found a reduced expression of MTND4 in CF cells. MTND4 is a mitochondrial gene encoding the MTND4 subunit of the mi...
متن کاملcompactifications and function spaces on weighted semigruops
chapter one is devoted to a moderate discussion on preliminaries, according to our requirements. chapter two which is based on our work in (24) is devoted introducting weighted semigroups (s, w), and studying some famous function spaces on them, especially the relations between go (s, w) and other function speces are invesigated. in fact this chapter is a complement to (32). one of the main fea...
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ژورنال
عنوان ژورنال: Redox Biology
سال: 2013
ISSN: 2213-2317
DOI: 10.1016/j.redox.2012.11.007