Fig. 3.

Fig. 3. Kinetin riboside stimulates β-catenin phosphorylation and degradation via a mechanism independent of GSK-3β. (A) HEK293-FL cells were treated with vehicle (DMSO) or kinetin riboside (10, 20, or 40 μM) in the presence of 0.75 μM BIO for 15 h, and FL activity was measured. Results are expressed as the mean ± SD of three independent experiments. *p < 0.05 and **p < 0.01, comparison between the BIO-treated control and kinetin riboside-treated groups. (B) HEK293-FL cells were treated with vehicle (DMSO) or kinetin riboside (10, 20, or 40 μM) in the presence of 0.75 μM BIO for 15 h. Cytosolic proteins were analyzed by Western blotting with anti-β-catenin antibody. (C) HEK293-FL cells were treated with vehicle (DMSO) or kinetin riboside (10, 20, or 40 μM) in the presence of 0.75 μM BIO for 15 h. Cytosolic proteins were analyzed by Western blotting with anti-active-β-catenin antibody. In (B) and (C), β-actin was used as a loading control, and β-catenin levels were normalized to those of β-actin. The bar graph indicates the average volume density corrected for the loading control, and results are expressed as the mean ± SD of three independent experiments. *p < 0.05 and **p < 0.01, comparison between the BIO-treated control and kinetin riboside-treated groups.

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