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. 2009 Apr 20;185(2):291–303. doi: 10.1083/jcb.200811105

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© 2009 Manzl et al.

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.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 6. — Caspase-2 processing is delayed in PIDD-deficient MEFs but still requires effector caspase activation. (A) Immortalized wild-type (wt) and pidd^−/− SV40-MEFs were exposed to 50 µg/ml etoposide (Eto) or 5 mJ/cm² UVR, and lysates were immunoblotted for caspase-2 processing, stripped, and reprobed with anti–active caspase-3 antibody followed by a reprobing with anti-GAPDH. (B) Wild-type and caspase-3/7 double-deficient SV40-MEFs were exposed to DNA damage as in A, and lysates were immunoblotted for caspase-2 processing. After detection of caspase-2, membranes were first stripped and reprobed with anti–active caspase-3 antibody followed by an antibody recognizing GAPDH to compare protein loading. Finally, membranes were stripped before detection of caspase-7.