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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

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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graphic file with name JCB9906130.f2a.jpg — Targeted disruption of the activated K-ras allele in cells derived from human colorectal carcinoma restores sensitivity to anoikis, and adhesion-dependent regulation of Bcl-X_L expression. (A) Analysis of apoptosis by cell death ELISA in DLD-1, DKS-8, and DKO-3 cells that were cultured in suspension overnight. Results represent the average of two independent experiments plus the SD. (B) Western blot analysis of Bcl-X_L was performed in cells that were cultured in monolayer (mon) or in suspension (susp) for the indicated time periods. Membranes were reprobed with an anti-CDK 4 antibody as a loading control.

graphic file with name JCB9906130.f2b.jpg — Targeted disruption of the activated K-ras allele in cells derived from human colorectal carcinoma restores sensitivity to anoikis, and adhesion-dependent regulation of Bcl-X_L expression. (A) Analysis of apoptosis by cell death ELISA in DLD-1, DKS-8, and DKO-3 cells that were cultured in suspension overnight. Results represent the average of two independent experiments plus the SD. (B) Western blot analysis of Bcl-X_L was performed in cells that were cultured in monolayer (mon) or in suspension (susp) for the indicated time periods. Membranes were reprobed with an anti-CDK 4 antibody as a loading control.