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The inositol 1,4,5-trisphosphate receptor regulates autophagy through its interaction with Beclin 1

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2009-07
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Vicencio, José Miguel
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The inositol 1,4,5-trisphosphate receptor regulates autophagy through its interaction with Beclin 1
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Author
  • Vicencio, José Miguel;
  • Ortíz, C.;
  • Criollo Céspedes, Alfredo;
  • Jones, A. W. E.;
  • Kepp, O.;
  • Galluzzi, Lorenzo;
  • Joza, N.;
  • Vitale, I.;
  • Morselli, E.;
  • Tailler, M.;
  • Castedo, M.;
  • Maiuri, M. C.;
  • Molgó, Jordi;
  • Szabadkai, G.;
  • Lavandero González, Sergio;
  • Kroemer, Guido;
Abstract
The inositol 1,4,5-trisphosphate receptor (IP3R) is a major regulator of apoptotic signaling. Through interactions with members of the Bcl-2 family of proteins, it drives calcium (Ca2+) transients from the endoplasmic reticulum (ER) to mitochondria, thereby establishing a functional and physical link between these organelles. Importantly, the IP3R also regulates autophagy, and in particular, its inhibition/depletion strongly induces macroautophagy. Here, we show that the IP3R antagonist xestospongin B induces autophagy by disrupting a molecular complex formed by the IP3R and Beclin 1, an interaction that is increased or inhibited by overexpression or knockdown of Bcl-2, respectively. An effect of Beclin 1 on Ca2+ homeostasis was discarded as siRNA-mediated knockdown of Beclin 1 did not affect cytosolic or luminal ER Ca2+ levels. Xestospongin B- or starvation-induced autophagy was inhibited by overexpression of the IP3R ligand-binding domain, which coimmunoprecipitated with Beclin 1. These results identify IP3R as a new regulator of the Beclin 1 complex that may bridge signals converging on the ER and initial phagophore formation.
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URI: https://repositorio.uchile.cl/handle/2250/121007
ISSN: 1350-9047
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CELL DEATH AND DIFFERENTIATION 16 (7): Special Issue: SI Pages: 1006-1017
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