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. 2006 Feb;17(2):770–778. doi: 10.1091/mbc.E05-08-0742

Figure 2.

Figure 2.

Disruption by insertional mutagenesis or targeted knockdown of eEF1A-1 in CHO cells confers palmitate-resistance. (A) Wild-type and eEF1A-1 mutant CHO cells were incubated with 500 μM palmitate (Palm), 80 nM staurosporine (Staur), 2 μM actinomycin D (Act D), 20 μM cycloheximde (Cyclo), or 10 μM camptothecin (Camp) for 24 h. Cell death was determined by propidium iodide staining and flow cytometry. (B) Cells were incubated as described in A. Apoptosis was determined by FragEL and flow cytometry. (C) Basal eEF1A-1 protein levels in whole cell lysates from wild-type CHO, eEF1A-1 mutant CHO, and stable CHO-derived cell lines expressing control siRNA (siRNA1) or siRNA directed against eEF1A-1 (siRNA2 and siRNA3) were detected by immunoblotting and quantified by densitometry. Inset is a representative blot. (D) Cell lines from C were incubated for 12 h with 500 μM palmitate. Cell death was determined by propidium iodide staining and flow cytometry. All data expressed as mean ± SEM for five independent experiments, *p < 0.05.