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. 2004 Jul;24(13):5821–5834. doi: 10.1128/MCB.24.13.5821-5834.2004

FIG. 6.

FIG. 6.

The synergistic enhancement of AR-dependent transactivation by Dyrk1A and Arip4 expression is independent of the kinase activity of Dyrk1A. (A) Dyrk1A with Arip4WT or Arip4Δ1165-1196 was expressed in CV-1 cells together with the MMTV-luciferase reporter gene. Cells were stimulated with the synthetic AR agonist R1881. Note that Arip4Δ1165-1196, which lacks the Dyrk1A substrate consensus sequence, was also able to enhance the effect of Dyrk1A. WT, wild type. (B) Arip4 with Dyrk1AWT or Dyrk1AK188R was expressed in CV-1 cells together with the MMTV-luciferase reporter gene. Cells were stimulated with the synthetic AR agonist R1881. Note that kinase-deficient mutant Dyrk1AK188R was able to stimulate AR-mediated activation not different from that stimulated by Dyrk1AWT. Luciferase activities were normalized to protein content, and ratios were expressed relative to those obtained with AR in the presence of R1881 (value set at 1; second bar from left in panels A and B). Means and SEMs for three independent experiments are shown. For comparisons indicated by brackets, one asterisk indicates a P value of <0.05 and three asterisks indicate a P value of <0.0001.