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. Author manuscript; available in PMC: 2016 Oct 21.
Published in final edited form as: Hum Mutat. 2008 May;29(5):640–647. doi: 10.1002/humu.20692

FIGURE 2.

FIGURE 2

Effect of the −36A>C genetic variant on human PLN promoter activity. A: Rat neonatal cardiomyocytes were transiently transfected with a luciferase expression vector driven by PLN-WT or PLN-MT (−36A>C) promoters, and were cultured in the absence (left) or presence (right) of 3 μM dexamethasone (Dex) for 45 hr. Transcriptional activity of the promoters was defined as a ratio of firefly luciferase activity to Renilla luciferase activity in the same cells, and normalized to the mean basal transcriptional activity of the promoter-less pGL3-basic vector. B: Sequence alignment of the normal and mutant human PLN upstream promoter regions. The relative positions of the promoter starting site (-1) and of the potential regulatory sequences (underlined) are indicated. The values are expressed as means±SEM (n=7). *P<0.05 vs. PLN-WT without Dex (two-way ANOVA and Student-Neuman-Keuls test). Polymorphism numbering is based on using the GenBank accession number AF177763.1for human PLN-sequence corresponding to proximal promoter and exon1as a reference.