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. 2009 Jul 24;284(39):26466–26481. doi: 10.1074/jbc.M109.027680

FIGURE 7.

FIGURE 7.

RNAi of CaMKIV accelerates RA induction of markers of neuronal differentiation in BE(2)C neuroblastoma cells. A, variation with time in mRNA levels of CaMKIV and differentiation markers by RNAi of CaMKIV, followed by RA treatment. BE(2)C cells were transfected for 24 h with 100 nm NSsi or 100 nm (total) CaMKIVsi-1/11, following which they were incubated in the absence (−; DMSO) or presence of 10 μm RA. At the indicated time points, mRNA abundances of CaMKIV, p21/Cip1, DCX, and peripherin were quantified by qRT-PCR. *, p < 0.05. B, variation with time in protein levels of CaMKIV by RNAi of CaMKIV followed by RA treatment. BE(2)C cells were transfected for 24 h with 100 nm NSsi or 100 nm (total) of CaMKIVsi-1/11, following which they were incubated in the absence (−; vehicle, DMSO), or presence (+), of 10 μm RA. At the indicated time points, protein levels of CaMKIV were analyzed by immunoblotting. The blot shown was also probed for GAPDH to confirm equivalent protein loading. C, variation with time in protein levels of differentiation markers by RNAi of CaMKIV followed by RA treatment. BE(2)C cells were treated as in B. At the indicated time points, protein levels of p21/Cip1, DCX, and vimentin were analyzed by immunoblotting. The blot shown was also probed for GAPDH to confirm equivalent protein loading.