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. 2015 Oct 20;47(12):634–643. doi: 10.1152/physiolgenomics.00082.2015

Fig. 2.

Fig. 2.

Mouse IGF-1 growth hormone-responsive element in intron 2 (in2GHRE) reporter constructs and their relative luciferase activities. A: a single copy of a 240 bp mouse IGF-1 in2GHRE fragment, either with wild-type sequence (WT GHRE clone 258) or with STAT5b mutated sequence (mut GHRE clone 268), was cloned upstream of human (hu) EF1a minimal promoter driving a CpG-free luciferase reporter gene (clone 256). Wild-type tandem STAT5b sites are shown as white and black rectangles and mutated sites as Xs. B: relative light units (RLU) compared with clone 294 in the presence or absence of growth hormone (GH) for the hu EF1a minimal promoter driving a CpG-free luciferase reporter (256), for the reporter construct plus the wild-type GHRE sequence (258), for the reporter construct with a mutated GHRE (268), or for the reporter construct with wild-type GHRE methylated at all 4 CpG sites (258meth).