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. Author manuscript; available in PMC: 2011 Aug 30.
Published in final edited form as: Mol Cell Endocrinol. 2010 May 26;325(1-2):143–149. doi: 10.1016/j.mce.2010.05.010

Figure 2.

Figure 2

Jak2 affects transcription of the RUSH gene.

Panel A. Prolactin increased (p < 0.001) progesterone-dependent transcription of a RUSH reporter construct (compare lanes 1 and 2). Inhibition of Jak2 phosphorylation by Tyrene CR4 (compare lanes 2 and 3), or mutation of the RUSH binding site (compare lanes 4 and 5), completely blocked (p < 0.001) the ability of prolactin to augment progesterone-dependent transcription of the same construct. Mean (± SEM) values with the same letter designation are not significantly different (p > 0.05). Serum-starved HRE-H9 cells were treated with ± R5020 for 16–20 hours ± Inhibitor ± prolactin for 5 minutes. This treatment of HRE-H9 cells applies to all outcomes in this figure.

Panel B. Phosphorylation of Jak2 had no effect (p > 0.05) on the total nuclear content of progesterone-induced RUSH evaluated by quantitative LSCM (details in section 2.6 of the Materials and Methods. Mean (± SEM) values with the same letter designation are not significantly different (p > 0.05).