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Cross talk between apoptosis and autophagy by caspase-mediated cleavage of Beclin 1

A Corrigendum to this article was published on 09 December 2010

Abstract

Beclin 1 has a key role in the initiation of autophagy, a process of self-cannibalism in which cytoplasmic constituents are sequestered and targeted for lysosomal degradation. In a recent issue of Cell Death & Disease, Wirawan et al. report the significant finding that caspases can cleave Beclin 1, thereby destroying its pro-autophagic activity. Moreover, the C-terminal fragment of Beclin 1 that results from this cleavage acquires a new function and can amplify mitochondrion-mediated apoptosis. Of note, the BH3 domain of Beclin 1 remains within the N-terminal fragment, which has no detectable pro-apoptotic activity. These findings provide important insights into the molecular cross talk between autophagy and apoptosis.

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Acknowledgements

This work was supported by funds from the EU 6th and 7th Framework Programs, as well as by grants from Ligue contre le Cancer (équipe labelisée), Agence Nationale pour la Recherche, Institut National sur le Cancer, Cancéropôle Ile-de-France and Fondation pour la Recherche Médicale (to GK) and by grant from Ligue contre le Cancer (to MD-M).

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Correspondence to M Djavaheri-Mergny or G Kroemer.

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Djavaheri-Mergny, M., Maiuri, M. & Kroemer, G. Cross talk between apoptosis and autophagy by caspase-mediated cleavage of Beclin 1. Oncogene 29, 1717–1719 (2010). https://doi.org/10.1038/onc.2009.519

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