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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 2006 Aug 18;103(36):13560. doi: 10.1073/pnas.0606689103

Correction for Austin et al., Death-receptor activation halts clathrin-dependent endocytosis

PMCID: PMC1569203

cell biology. For the article “Death-receptor activation halts clathrin-dependent endocytosis,” by Cary D. Austin, David A. Lawrence, Andrew A. Peden, Eugene E. Varfolomeev, Klara Totpal, Ann M. De Mazière, Judith Klumperman, David Arnott, Victoria Pham, Richard H. Scheller, and Avi Ashkenazi, which appeared in issue 27, July 5, 2006, of Proc. Natl. Acad. Sci. USA (103, 10283–10288; first published June 26, 2006; 10.1073/pnas.0604044103), the authors note that in Fig. 2, the immunoblots corresponding to the bottom of panels b and c are reversed. The corrected figure and its legend appear below. This error does not affect the conclusions of the article.

Fig. 2.

Fig. 2.

Involvement of different caspases in cleavage of AP2α and CHC. (a) BJAB cells were treated with the pan-caspase inhibitor zVAD-fmk (20 μM, 30 min) followed by treatment with crosslinked Apo2L/TRAIL (1 μg/ml) and analyzed by immunoblot for processing of caspase-8, caspase-3, AP2α, and CHC. Arrows with open heads indicate cleavage products, and arrows with filled heads indicate full-length proteins. (b–d) Bax−/− or Bax+/− HCT116 cells or caspase-3-deficient MCF-7 cells were treated with Apo2L/TRAIL and analyzed as in a.


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