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AKAP12β Reactivation in Glioblastoma Cells via Demethylating Drug Treatment

Reactivation of AKAP12β in primary glioblastoma cells (NCH82, NCH89, NCH440) by 5-aza-2’-deoxycytidine treatment for 72h. Evaluation of AKAP12β transcript expression relative to ACTB, GAPDH, and HPRT1.

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AKAP12β Reactivation in Glioblastoma Cells via Demethylating Drug Treatment

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  1. Supplemental Figure 9. Reactivation of AKAP12β in primary glioblastoma cells by demethylating drug treatment. Primary glioblastoma cell lines NCH82, NCH89 and NCH440 were treated with 0 µmol/l (-DAC) or 2 µmol/l (+DAC) 5-aza-2’-deoxycytidine for 72h (see also Fig. 8). Re-expression of AKAP12β transcript relative to ACTB, GAPDH and HPRT1 after 72 h 5-aza-2’-deoxycytidine treatment.

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