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. 2013 Aug 1;24(15):2477–2490. doi: 10.1091/mbc.E13-01-0067

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© 2013 Teske et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 7: — shRNA knockdown of NOXA protects cells from stress induced by MG132 treatment. (A) WT and ATF5-KD2 MEF were treated with 1 μM MG132 for 8 h or no treatment (NT). The mRNA levels for CHOP, ATF5, NOXA, TXNIP, and APAF1 were measured by qPCR. In addition, NOXA mRNA was measured in ATF5-KD1 cells as indicated. *Statistical significance (p < 0.05) with respect to the untreated control. ^#Difference between cell types. (B) MEF cells expressing an shRNA targeting NOXA or scramble control were treated for 8 h with MG132. The last two digits in the validated shRNA identification number are listed. Relative NOXA mRNA levels were measured by qPCR. *Statistical significance (p < 0.05). (C) WT, CHOP^−/−, and NOXA-KD MEF cells were treated with 1 μM MG132 for 24 h, and cell death was determined as the percentage of viable cells as measured by MTT assay upon MG132 treatment compared with untreated controls. (D) WT and TXNIP-KD MEF cells were treated with 1 μM MG132 for 12 h, and the relative level of TXNIP mRNA was measured by qPCR. (E) Death of WT and TXNIP-KD cells was measured as the percentage of viable cells as determined by MTT assays after 24 h of MG132 treatment compared with untreated controls.