Mutations in the first intron of the SHR renin gene disrupt putative regulatory elements

Clinical and Experimental Pharmacology & Physiology
H YuA Wilks

Abstract

1. Four single base mutations unique to the spontaneously hypertensive rat (SHR) were identified in the first 1100 base pairs of its renin gene first intron when compared to that of Wistar-Kyoto and Sprague-Dawley normotensive rats. 2. These mutations were found to fall within the consensus sequences for a number of transcription factors and thus may alter the affinity of these putative transcription factor binding sites. 3. The reported overexpression of the renin gene in the SHR may therefore result from these structural abnormalities and, in turn, result in a tissue angiotensin-dependent hypertension in this strain.

References

Jan 11, 1992·Nucleic Acids Research·S Faisst, S Meyer
Apr 1, 1990·The Journal of Clinical Investigation·T W KurtzB L Hjelle
May 20, 1988·Journal of Molecular Biology·A FukamizuK Murakami

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Citations

Aug 10, 2010·Nucleic Acids Research·Julia Yue CuiCurtis D Klaassen
Mar 21, 1998·Clinical and Experimental Hypertension : CHE·R Di NicolantonioA Wilks
Apr 25, 2000·American Journal of Hypertension·P LantelmeJ Sassard

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