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. Author manuscript; available in PMC: 2010 Mar 17.
Published in final edited form as: Science. 2009 Jun 26;324(5935):1713–1716. doi: 10.1126/science.1171721

Figure 2. Localization of STAT3 to mitochondria supports Ras transformation.

Figure 2

(A) Fractionation of cells mechanically disrupted in absence of detergent and separated into P100 (plasma membrane), S100 (organelle-free cytosol), and mitochondrial fractions. Samples probed for STAT3, IGF1-R1α, or Bcl-XL, as indicated. (B) Distribution of STAT3 mutants expressed in H-RasV12-transduced cells. Erk1/2 and Bcl-XL expression verified fraction purity. (C) Protease-sensitivity of proteins associated with mitochondrial membranes in absence (unt) or presence of proteinase K (+PK) or proteinase K and Triton X-100 (+PK/T). (D) Survival of H-RasV12 expressing cells following glucose depletion. Survival of STAT3-null (KO) or wild type cells expressing H-RasV12 (WT) or STAT3-null cells expressing H-RasV12 reconstituted with empty vector (EV) or STAT3 mutants after growth in low or high glucose medium, as indicated. Asterisks indicate statistically significant differences (p<.05 by student’s t-test) of individual conditions relative to empty vector. (E) Survival of cells exposed to 2% oxygen. (F) Mitochondrially-targeted wild type and mutant STAT3 protein expression. (G) Colony formation by H-RasV12-, (H) v-Src-, and (I, J) N- and K-Ras-expressing cell lines.