Figure 5

Blockade of translation with anisomycin (Ani, 10 μM) selectively altered the TSA-induced regulation of PKMζ and PKCζ expression, while epigenetically-driven upregulation of PKCλ expression was unaffected. (a) Application of Ani did not impair the TSA-induced upregulation of PKCλ expression. Control, TSA-treated (19 h) cultures and cultures treated with Ani alone (20 h) or in combinations with TSA were used for comparisons. For the last group, Ani was administered for 1 h before the application of TSA. [F_(3,17) = 20,913; p < 0,001; n = 5–6/group]. (b,c) Ani prevented downregulation of PKMζ expression in TSA-treated cultures [KW: H (3, N = 24) = 13,22000 p = 0,0042; *p = 0,002; ^&p < 0,001; n = 6/group] and significantly alleviated epigenetically-driven upregulation of PKCζ expression [KW: H (3, N = 20) = 16,45893 p = 0,0009; *p < 0,001; n = 5/group]. Representative experiment below demonstrates patterns of PKCζ expression in the current experimental series. mRNA levels were determined by standard PCR followed by agarose gel electrophoresis. YWHAZ served as a reference. *Significant differences; ^&Significant difference (relative to standard control group); ns – not significant.