A common variant in the proximal promoter of the angiotensinogen gene, an adenine instead of a guanine at position -6, is associated with essential hypertension and significantly increases basal transcription in vitro.
p-value: p=2.4 x 10^-6
In earlier studies, we provided statistical evidence that individual differences in the angiotensinogen gene, the precursor of the vasoactive hormone angiotensin II, constitute inherited predispositions to essential hypertension in humans. We have now identified a common variant in the proximal promoter, the presence of an adenine, instead of a guanine, 6 bp upstream from the initiation site of transcription, in significant association with the disorder. Tests of promoter activity and DNA binding studies with nuclear proteins suggest that this nucleotide substitution affects the basal transcription rate of the gene. These observations provide some biological insight about the possible mechanism of a genetic predisposition to essential hypertension; they may also have important evolutionary implications.
Inoue et al. (Tue,) conducted a other in Essential hypertension (n=547). Adenine at position -6 (A(-6)) in AGT promoter vs. Guanine at position -6 (G(-6)) was evaluated on Basal transcription rate in vitro (p=2.4 x 10^-6). A common variant in the proximal promoter of the angiotensinogen gene, an adenine instead of a guanine at position -6, is associated with essential hypertension and significantly increases basal transcription in vitro.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: