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Cited by 482

The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.

Apoptosis blocks Beclin 1-dependent autophagosome synthesis: an effect rescued by Bcl-xL

Open access
Luo, S, Rubinsztein, D C·2010·Cell Death & Differentiation

Abstract

Apoptotic cell death is mediated by caspase activation. Autophagy involves the sequestration of cytoplasmic contents into autophagosomes for traffic to lysosomes for degradation. Although autophagy is antiapoptotic, increased numbers of autophagosomes have been associated with forms of non-apoptotic cell death. Apoptosis and autophagy may be co-regulated in the same directions, as the antiapoptotic Bcl-2 and Bcl-xL proteins negatively regulate autophagy by binding to Beclin 1 (mammalian Atg6), and proapoptotic BH3-only proteins may reverse this effect by displacing these interactions. Here, we show that apoptosis can suppress autophagy. Apoptosis induced by the proapoptotic protein Bax reduced autophagy by enhancing caspase-mediated cleavage of Beclin 1 at D149. After cleavage, both N- and C-terminal Beclin 1 fragments change their localisations and these fragments do not interact normally with Vps34, which is required for autophagy. The cleavage of Beclin 1 is a critical event whereby caspases inhibit autophagy, as a non-cleavable Beclin 1 mutant restored autophagy in cells overexpressing Bax.

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Metadata

Authors
Luo, S., & Rubinsztein, D. C.
Venue
Cell Death & Differentiation
Published
2009-08-28
Volume
17
Issue
2
Pages
268-277
ISSN
  • 1350-9047 (ISSN-L)
  • 1476-5403
OpenAlex
W2145434871
Cited by
482
References
35
FWCI
17.89
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Apoptosis blocks Beclin 1-dependent autophagosome synthesis: an effect rescued by Bcl-xL. https://app.cochat.ai/papers/10.1038/cdd.2009.121
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Luo, S., & Rubinsztein, D. C. (2010). Apoptosis blocks Beclin 1-dependent autophagosome synthesis: an effect rescued by Bcl-xL. Cell Death & Differentiation. https://doi.org/10.1038/cdd.2009.121

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