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. Author manuscript; available in PMC: 2014 May 12.
Published in final edited form as: Sci Transl Med. 2013 Oct 30;5(209):209ra152. doi: 10.1126/scitranslmed.3006839

Fig. 2. Bcl2L12-specific SNAs promote apoptotic signaling in glioma cells.

Fig. 2

(A and B) Bcl2L12 knockdown by siL12-SNAs sensitizes cells to apoptosis (measured by caspase-3 and caspase-7 cleavage) upon treatment with staurosporine (STS) and temozolomide (TMZ). LS, large subunit; LS+N, large subunit plus N-peptide. (C) Effect of Bcl2L12 knockdown on p53 protein stability, phosphorylated p53 (p-p53Ser15), and the p53 target p21 upon doxorubicin (Doxo) treatment for the indicated times. (D) p53 target gene induction of p21 on the mRNA level as measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). (E) Bcl2L12 mRNA knockdown was assessed in parallel and expressed as fold change relative to siCo-SNA–treated cells at 0, 4, 8, and 16 hours after application of doxorubicin. Data are means ± SD (n = 3).