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Apoptosis

A lethal injection

Nature Reviews Molecular Cell Biology volume 4, page 345 (2003)Cite this article

Much is known about GrB — there's evidence that it kills with or without caspase activation, and that it causes mitochondrial permeabilization with or without members of the Bcl-2 family. So Froelich and co-workers set out to assess the relative contributions of these pathways, to come up with a probable scheme for how GrB normally acts. To do this, they measured several different hallmarks of apoptosis — loss of mitochondrial membrane potential (ψm), DNA fragmentation and activation of procaspase precursors.

Most previous studies have been done on cell lysates, after GrB has been delivered to its target. By contrast, Froelich and colleagues studied whole cells after delivery of the physiological form of GrB, a GrB– Serglycin (SG) complex. Previous studies with lysates had indicated that GrB-treated cells rapidly acquire cleaved (and presumably active) procaspase-3. Mature caspase-3 and GrB then process caspase-7 to complete the initial phase of apoptosis. The authors therefore asked how the absence of procaspase-3 might alter the pattern of apoptosis in whole cells after delivery of GrB–SG.

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ORIGINAL RESEARCH PAPER

  1. Metkar, S. S. et al. Granzyme B activates procaspase-3 which signals a mitochondrial amplification loop for maximal apoptosis. J. Cell Biol. 160, 875–885 (2003)

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Authors
  1. Alison Mitchell
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Mitchell, A. A lethal injection. Nat Rev Mol Cell Biol 4, 345 (2003). https://doi.org/10.1038/nrm1112

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  • DOI: https://doi.org/10.1038/nrm1112

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