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  Indian J Med Microbiol
 

Figure 3: Blockade of CK2α antagonized the effects of brain-derived neurotrophic factor on serum response element-mediated reporter expression, serum response factor phosphorylation, and Mcl-1 mRNA expression. PC12 cells (2 × 105/cm2) were cotransfected with pGL2-5x serum response element-SV40pr plasmid (0.5 μg) and CK2α siRNA (16 pmole) for 48 h, followed by 10 ng/mL of brain-derived neurotrophic factor treatment for 6 h. The cells were harvested for (a) a luciferase activity assay by using the Dual-Glo Luciferase Assay System or cell lysates were prepared for a Western blot analysis of (b) serum response factor phosphorylation at Ser99 and (c) Mcl-1 mRNA by using real-time quantitative polymerase chain reaction (n = 8-12 in each group from three independent batches of cultures). Data are expressed as mean ± standard deviation. Statistical significance was evaluated using a one-way ANOVA, followed by the Newman–Kuel method. ***P < 0.001

Figure 3: Blockade of CK2α antagonized the effects of brain-derived neurotrophic factor on serum response element-mediated reporter expression, serum response factor phosphorylation, and <i>Mcl-1</i> mRNA expression. PC12 cells (2 × 10<sup>5</sup>/cm<sup>2</sup>) were cotransfected with pGL2-5x serum response element-SV40pr plasmid (0.5 μg) and CK2α siRNA (16 pmole) for 48 h, followed by 10 ng/mL of brain-derived neurotrophic factor treatment for 6 h. The cells were harvested for (a) a luciferase activity assay by using the Dual-Glo Luciferase Assay System or cell lysates were prepared for a Western blot analysis of (b) serum response factor phosphorylation at Ser99 and (c) <i>Mcl-1</i> mRNA by using real-time quantitative polymerase chain reaction (<i>n</i> = 8-12 in each group from three independent batches of cultures). Data are expressed as mean ± standard deviation. Statistical significance was evaluated using a one-way ANOVA, followed by the Newman–Kuel method. ***<i>P</i> < 0.001