ArticleBMC genetics2007
Sequence analysis of coding and 3' and 5' flanking regions of the epithelial sodium channel alpha, beta, and gamma genes in Dahl S versus R rats.
Article in BMC genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Role of the epithelial sodium channel in salt-sensitive hypertension.Acta pharmacologica Sinica · 2011Review
- The Alternatively Spliced Form "b" of the Epithelial Sodium Channel α subunit (α ENaC): Any Prior Evidence of its Existence?Clinical Medicine Insights. Cardiology · 2010Article
- The Epithelial Sodium Channel alpha subunit (alpha ENaC) alternatively spliced form "b" in Dahl rats: What's next?International archives of medicine · 2010Article
- Characterization of the epithelial sodium channel alpha subunit coding and non-coding transcripts and their corresponding mRNA expression levels in Dahl R versus S rat kidney cortex on normal and high salt diet.International archives of medicine · 2009Article
- Important genetic checkpoints for insulin resistance in salt-sensitive (S) Dahl rats.Cardiovascular diabetology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo test whether epithelial sodium channel (ENaC) genes' variants contribute to salt sensitive hypertension in Dahl rats, we screened ENaC alpha, beta, and gamma genes entire coding regions, intron-exon junctions, and the 3' and 5' flanking regions in Dahl S, R and Wistar rats using both Denaturing High Performance Liquid Chromatography (DHPLC) and sequencing.
resultsOur analysis revealed no sequence variability in the three genes encoding ENaC in Dahl S versus R rats. One homozygous sequence variation predicted to result in a D75E substitution was identified in Dahl and Wistar rat ENaC alpha compared to Brown Norway. Six and two previously reported polymorphic sites in Brown Norway sequences were lost in Dahl and Wistar rats, respectively. In the 5' flanking regions, we found a deletion of 5GCTs in Dahl and Wistar rat ENaC alpha gene, five new polymorphic sites in ENaC beta and gamma genes, one homozygous sequence variation in Dahl and Wistar rat ENaC gamma gene, as well as one Dahl rat specific homozygous insertion of -1118CCCCCA in ENaC gamma gene. This insertion created additional binding sites for Sp1 and Oct-1. Five and three Brown Norway polymorphic sites were lost in Dahl and Wistar rats, respectively. No sequence variability in ENaC 3' flanking regions was identified in Dahl compared to Brown Norway rats.
conclusionThe first comprehensive sequence analysis of ENaC genes did not reveal any differences between Dahl S and R rats that were isogenic in the regions screened. Mutations in ENaC genes intronic sequence or in ENaC-regulatory genes might possibly account for increased ENaC activity in Dahl S versus R rats.
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