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. Author manuscript; available in PMC: 2006 Nov 7.
Published in final edited form as: Mol Cell Endocrinol. 2005 Jul 15;239(1-2):45–53. doi: 10.1016/j.mce.2005.04.006

Fig. 3.

Fig. 3

PRL responsiveness localizes to the −254 to −180 promoter region. (A) Diagram of the cyclin D1 promoter showing the length of promoter truncations and the relative position of selected transcription factor binding sites. (B) CHO cells were transiently transfected with PRLR, β-galactosidase and truncated cyclin D1 promoter reporter constructs D1Δ-944, D1Δ-304, D1Δ-254, D1Δ-180 or D1Δ-71. Transfected cells were cultured in serum-free media with (solid bar) or without (open bar) 10 nM PRL. After 24 h, samples were assayed for luciferase activity. β-Galactosidase activity was used to correct for transfection efficiencies, and activity was presented relative to the untreated D1Δ-944-transfected cells. Data represent the mean of at least three separate experiments ± S.E.M. Numbers above solid bars denote the fold change compared to untreated control and asterisks indicate a statistically significant increase in PRL-treated promoter activity compared with non-PRL-treated control (*P<0.05, ***P<0.001) using ANOVA with Bonferroni post-test.