IKK connects autophagy to major stress pathways

Alfredo Criollo, Laura Senovilla, Hélène Authier, Maria Chiara Maiuri, Eugenia Morselli, Ilio Vitale, Oliver Kepp, Ezgi Tasdemir, Lorenzo Galluzzi, Si Shen, Maximilien Tailler, Nicolas Delahaye, Antoine Tesniere, Daniela De Stefano, Aména Ben Younes, Francis Harper, Gérard Pierron, Sergio Lavandero, Laurence Zitvoge, Alain IsraelVéronique Baud, Guido Kroemer

Research output: Contribution to journalArticlepeer-review


Cells respond to stress by activating cytoplasmic mechanisms as well as transcriptional programs that can lead to adaptation or death. Autophagy represents an important cytoprotective response that is regulated by both transcriptional and transcription-independent pathways. NFκB is perhaps the transcription factor most frequently activated by stress and has been ascribed with either pro- or anti-autophagic functions, depending on the cellular context. Our results demonstrate that activation of the IKK (IκB kinase) complex, which is critical for the stress-elicited activation of NFκB, is sufficient to promote autophagy independent of NFκB, and that IKK is required for the optimal induction of autophagy by both physiological and pharmacological autophagic triggers.

Original languageEnglish
Pages (from-to)189-191
Number of pages3
Issue number1
Publication statusPublished - Jan 1 2010


  • AMPK
  • JNK1
  • mTOR
  • Nutrient deprivation
  • Rapamycin

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology


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