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. 2000 Apr 17;149(2):447–456. doi: 10.1083/jcb.149.2.447

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© 2000 The Rockefeller University Press

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graphic file with name JCB9906130.f3a.jpg — Activated ras inhibits downregulation of Bcl-X_L and apoptosis in IEC-18 cells treated with cytochalasin D (CD). (A) Microphotographs of IEC-18 and IEC-ras-3 cells that were grown in monolayer with and without treatment with 10 μg/ml of CD for 16 h. (B) Western blot analysis of Bcl-X_L in IEC-18 and IEC-ras-3 cells that were grown in monolayer with (+) and without (−) treatment with CD for 16 h. Membranes were reprobed with anti-CDK 4 antibody as a loading control. (C) Analysis of apoptosis by cell death ELISA in IEC-18 and IEC-ras-3 cells grown in monolayer with (+) and without (−) treatment with 10 μg/ml of CD for 16 h. A similar volume of DMSO (vehicle) was added to the untreated cells. Results represent the average of three independent experiments plus the SEM.

graphic file with name JCB9906130.f3b.jpg — Activated ras inhibits downregulation of Bcl-X_L and apoptosis in IEC-18 cells treated with cytochalasin D (CD). (A) Microphotographs of IEC-18 and IEC-ras-3 cells that were grown in monolayer with and without treatment with 10 μg/ml of CD for 16 h. (B) Western blot analysis of Bcl-X_L in IEC-18 and IEC-ras-3 cells that were grown in monolayer with (+) and without (−) treatment with CD for 16 h. Membranes were reprobed with anti-CDK 4 antibody as a loading control. (C) Analysis of apoptosis by cell death ELISA in IEC-18 and IEC-ras-3 cells grown in monolayer with (+) and without (−) treatment with 10 μg/ml of CD for 16 h. A similar volume of DMSO (vehicle) was added to the untreated cells. Results represent the average of three independent experiments plus the SEM.