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MUTATIONS IN THE FIRST INTRON OF THE SHR RENIN GENE DISRUPT PUTATIVE REGULATORY ELEMENTS
Author(s) -
Yu H.,
Nicolantonio R. Di,
Lan L.,
Wilks A.
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02040.x
Subject(s) - gene , renin–angiotensin system , intron , biology , genetics , transcription factor , transcription (linguistics) , regulatory sequence , mutation , microbiology and biotechnology , endocrinology , blood pressure , linguistics , philosophy
SUMMARY 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.