Skip to main content
. Author manuscript; available in PMC: 2013 Jun 16.
Published in final edited form as: J Mol Endocrinol. 2008 May;40(5):211–229. doi: 10.1677/JME-07-0156

Fig. 2.

Fig. 2

Transcriptional responses to ERβs from heterologous reporter systems. (A) Responses from the ERE-dependent signaling pathway. MDA-MB-231 or HeLa cells were transiently transfected with an expression vector bearing none (V), ERβ or ERβEBD cDNA together with a reporter vector bearing the TFF1 or C3 gene promoter in the absence or presence of 10−9 M E2 for 24h. Normalized luciferase values represented as fold changes compared with the luciferase values obtained with control vector in absence of E2, which was set to 1. Shown are the mean ± SEM of three independent experiments performed in duplicate. (B) Transactivation ability of ERβEBD in simulated ERE-independent signaling pathways. MDA-MB-231, HeLa, or U-2 OS cells were transiently transfected with an expression vector bearing ERβ or ERβEBD cDNA together with reporter vector bearing the MMP1 gene or the RARA gene proximal promoter. Cells were treated without or with 10−9 M E2, 10−8 DPN, 10−7 M 4-OHT or ICI for 40h. Normalized luciferase values are represented as fold change compared with the luciferase values obtained without ligand. Results are the mean ± SEM of three independent experiments performed in triplicate.