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Literature DB >> 11406278

Analysis of the mouse Scnn1a promoter in cortical collecting duct cells and in transgenic mice.

S Kohler¹, S Pradervand, C Verdumo, A M Mérillat, M Bens, A Vandewalle, F Beermann, E Hummler.

Abstract

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.

Entities: Disease Gene Species

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Year: 2001 PMID： 11406278 DOI： 10.1016/s0167-4781(01)00228-7

Source DB: PubMed Journal: Biochim Biophys Acta ISSN： 0006-3002

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Cited

10 in total

1. Dot1a-AF9 complex mediates histone H3 Lys-79 hypermethylation and repression of ENaCalpha in an aldosterone-sensitive manner.

Authors: Wenzheng Zhang; Xuefeng Xia; Mary Rose Reisenauer; Charles S Hemenway; Bruce C Kone
Journal: J Biol Chem Date: 2006-04-24 Impact factor: 5.157

10. Physical and functional interaction of Rnf2 with Af9 regulates basal and aldosterone-stimulated transcription of the α-ENaC gene in a renal collecting duct cell line.

Authors: Zhi-Yuan Yu; Qun Kong; Bruce C Kone
Journal: Biosci Rep Date: 2013-10-25 Impact factor: 3.840

10 in total

Analysis of the mouse Scnn1a promoter in cortical collecting duct cells and in transgenic mice.

1. Dot1a-AF9 complex mediates histone H3 Lys-79 hypermethylation and repression of ENaCalpha in an aldosterone-sensitive manner.

2. Mineralocorticoid receptor antagonizes Dot1a-Af9 complex to increase αENaC transcription.

Review 3. Epigenetics and the control of the collecting duct epithelial sodium channel.

4. Sp1 trans-activates and is required for maximal aldosterone induction of the αENaC gene in collecting duct cells.

5. Regulation of αENaC expression by the circadian clock protein Period 1 in mpkCCD(c14) cells.

6. Aldosterone-sensitive repression of ENaCalpha transcription by a histone H3 lysine-79 methyltransferase.

7. An Af9 cis-element directly targets Dot1a to mediate transcriptional repression of the αENaC gene.

8. Aldosterone reprograms promoter methylation to regulate αENaC transcription in the collecting duct.

9. Aldosterone and vasopressin affect {alpha}- and {gamma}-ENaC mRNA translation.

10. Physical and functional interaction of Rnf2 with Af9 regulates basal and aldosterone-stimulated transcription of the α-ENaC gene in a renal collecting duct cell line.