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. 2008 Oct 17;283(42):28660–28669. doi: 10.1074/jbc.M802645200

FIGURE 4.

FIGURE 4.

Dyrk1A inhibits the role of ASF in tau exon 10 inclusion. a, overexpression of Dyrk1A inhibited the role of ASF in tau exon 10 inclusion. Mini-tau gene pCI-SI9/LI10 was co-transfected with ASF or Dyrk1A into COS7 cells for 48 h, and the total RNA was extracted and subjected for measurement of tau exon 10 splicing by using RT-PCR. Con, control. b, knock down of Dyrk1A by its siRNA elevated exon 10 inclusion induced by ASF. Mini-tau gene was co-transfected into HEK-293T cells with ASF and siRNA of Dyrk1A or its scrambled form, and then tau exon 10 splicing was analyzed by RT-PCR after a 48-h transfection. Expression of endogenous Dyrk1A was decreased by siRNA of Dyrk1A dose-dependently (inset panel). Transfection of Dyrk1A siRNA significantly increased the 4R-tau expression when compared with the scrambled form. c, inhibition of Dyrk1A increased 4R-tau expression in differentiated human neuronal progenitor cells. Human neuronal progenitor cells were differentiated with retinoid acid for 6 days and then treated with 12.5 μm EGCG or 10 μm Harmine for 24 h to inhibit Dyrk1A. The cell lysates were objected to Western blots with anti-3R-tau and anti-4R-tau antibodies. The ratio of 4R-tau and 3R-tau was calculated. The data are presented as mean ± S.D. d, Dyrk1A drove ASF into speckles. HA-ASF and/or Dyrk1A or Dyrk1AK188R were co-transfected into HeLa cells. After a 48-h transfection, the cells were fixed and immunostained by anti-HA and anti-Dyrk1A and followed by TRITC-anti-rabbit IgG or FITC-anti-mouse IgG, respectively. Hoechst was used for nucleus staining. **, p < 0.01 versus control group, #, p < 0.05 versus ASF group.