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. 2004 Oct 15;114(8):1117–1127. doi: 10.1172/JCI22222

Figure 3.

Figure 3

Modulation of mitochondrial survivin during the cellular stress response. (A) Regulation of survivin by hypoxia. HeLa cells were exposed to hypoxia, and analyzed by immunoblotting followed by densitometry. N, normoxic cultures; H, hypoxic cultures. (B) Subcellular fractionation. Cytosolic or mitochondrial fractions from HeLa cells were exposed to hypoxia, and analyzed by immunoblotting. (C) Cycloheximide block. Normoxic or hypoxic HeLa cells were treated with cycloheximide, and analyzed by immunoblotting at the indicated time intervals. Lower panel: β-Actin–normalized densitometric quantification of differential survivin stability in control versus hypoxic conditions. (D) Modulation by DNA damage. Untreated (None) or MCF-7 cells treated with nonapoptotic concentrations of adriamycin (Adriam) were fractionated in cytosolic and mitochondrial fractions, and analyzed by immunoblotting.

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