Analysis of the mouse Scnn1a promoter in cortical collecting duct cells and in transgenic mice.
We have isolated and characterised the promoter of the mouse Scnn1a (alpha ENaC) gene. Using transient transfections of serial deletion mutants into Scnn1a-expressing cells, we demonstrate that 1.56 kb of 5' upstream sequence is required for cell-specific expression and corticosteroid-mediated regulation. These 5' sequences are not sufficient to drive expression of a lacZ reporter gene or a rat Scnn1a cDNA in transgenic mice, where they failed to rescue Scnn1a deficiency.
Kohler
S
S
Institute of Pharmacology and Toxicology, University of Lausanne, Switzerland.
Pradervand
S
S
Verdumo
C
C
Mérillat
A M
AM
Bens
M
M
Vandewalle
A
A
Beermann
F
F
Hummler
E
E
D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D002478:Cells, Cultured; D016384:Consensus Sequence; D053503:Epithelial Sodium Channels; D005786:Gene Expression Regulation; D007672:Kidney Cortex / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000378:metabolism*; D051379:Mice; D008822:Mice, Transgenic; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic; D015222:Sodium Channels / Q000235:genetics*; D014162:Transfection
D053503:Epithelial Sodium Channels; C507047:Scnn1a protein, mouse; D015222:Sodium Channels