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. 2005 Aug 10;102(34):12117–12122. doi: 10.1073/pnas.0409097102

Fig. 3.

Fig. 3.

N-Myc directly regulates transcription of the identified genes. (A) mRNA expression of N-Myc in SK-N-BE and SK-N-BE9N cells as a function of RA treatment. (B) Expression of the N-Myc protein in SK-N-BE and SK-N-BE9N cells by Western blotting. The levels of Myc protein were normalized to β-actin. (C) Northern blotting analysis of genes in SK-N-BE versus SK-N-BE9N cells treated with RA for 0, 7, and 14 days. (D and E) mRNA expression analysis performed in SH-SY-5Y and HL-60 cells. The latter were differentiated with DMSO for 0, 1, and 3 days. (F) Expression level of N-Myc protein in Tet-21/N cells after treatment with tetracycline (TET). (G) Relative expression of N-Myc and target genes at different time points of tetracycline treatment by real-time PCR. (H and I) Repression of c-Myc by RNA interference in HEK-293 cells using specific C-MYC small interfering RNAs (siRNAs) (Ambion). Negative control was performed with a silencer duplex RNA (control siRNA lane). c-Myc protein was detected by Western blot and quantified by densitometric analysis. (J) Measurement of mRNA expression of c-MYC and tested genes by real-time PCR in HEK-293 cells.