Year: 2010
Type: editorial
Abstract: 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. NFkappaB 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 (IkappaB kinase) complex, which is critical for the stress-elicited activation of NFkappaB, is sufficient to promote autophagy independent of NFkappaB, and that IKK is required for the optimal induction of autophagy by both physiological and pharmacological autophagic triggers.
Source: Autophagy
Authors: Alfredo Criollo, Laura Senovilla, Hélène Authier, Maria Chiara Maiuri, Eugenia Morselli, Ilio Vitale, Oliver Kepp, Ezgi Tasdemir, Lorenzo Galluzzi, Shensi Shen, Maximilien Tailler, Nicolas Delahaye, Antoine Tesnière, Daniela De Stefano, Amena BenYounès, Francis Harper, Gérard Pierron, Sergio Lavandero, Laurence Zitvogel, Alain Israel, Véronique Baud, Guido Kroemer
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2004810412