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The IKK complex contributes to the induction of autophagy

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2010-02-03
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Criollo Céspedes, Alfredo
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The IKK complex contributes to the induction of autophagy
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Author
  • Criollo Céspedes, Alfredo;
  • Senovilla, Laura;
  • Authier, Helene;
  • Maiuri, M. C.;
  • Morselli, E.;
  • Vitale, I.;
  • Kepp, O.;
  • Tasdemir, E.;
  • Galluzzi, Lorenzo;
  • Shen, S.;
  • Tailler, M.;
  • Delahaye, N.;
  • Tesniere, A.;
  • De Stefano, D.;
  • Ben Younes, Amena;
  • Harper, F.;
  • Pierron, G.;
  • Lavandero González, Sergio;
  • Zitvogel, L.;
  • Israel, A;
  • Baud, V;
  • Kroemer, Guido;
Abstract
In response to stress, cells start transcriptional and transcription-independent programs that can lead to adaptation or death. Here, we show that multiple inducers of autophagy, including nutrient depletion, trigger the activation of the IKK (I kappa B kinase) complex that is best known for its essential role in the activation of the transcription factor NF-kappa B by stress. Constitutively active IKK subunits stimulated autophagy and transduced multiple signals that operate in starvation-induced autophagy, including the phosphorylation of AMPK and JNK1. Genetic inhibition of the nuclear translocation of NF-kappa B or ablation of the p65/RelA NF-kappa B subunit failed to suppress IKK-induced autophagy, indicating that IKK can promote the autophagic pathway in an NF-kappa B-independent manner. In murine and human cells, knockout and/or knockdown of IKK subunits (but not that of p65) prevented the induction of autophagy in response to multiple stimuli. Moreover, the knockout of IKK-beta suppressed the activation of autophagy by food deprivation or rapamycin injections in vivo, in mice. Altogether, these results indicate that IKK has a cardinal role in the stimulation of autophagy by physiological and pharmacological stimuli.
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URI: https://repositorio.uchile.cl/handle/2250/120999
ISSN: 0261-4189
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EMBO JOURNAL 29 (3): 619-631
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