IKK connects autophagy to major stress pathways.
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.
Criollo
Alfredo
A
INSERM, U848, Villejuif, France.
Senovilla
Laura
L
Authier
Hélène
H
Maiuri
Maria Chiara
MC
Morselli
Eugenia
E
Vitale
Ilio
I
Kepp
Oliver
O
Tasdemir
Ezgi
E
Galluzzi
Lorenzo
L
Shen
Shensi
S
Tailler
Maximilien
M
Delahaye
Nicolas
N
Tesniere
Antoine
A
De Stefano
Daniela
D
Younes
Aména Ben
AB
Harper
Francis
F
Pierron
Gérard
G
Lavandero
Sergio
S
Zitvogel
Laurence
L
Israel
Alain
A
Baud
Véronique
V
Kroemer
Guido
G
D000818:Animals; D001343:Autophagy / Q000235:genetics / Q000502:physiology*; D006801:Humans; D051550:I-kappa B Kinase / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D008954:Models, Biological; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D013312:Stress, Physiological / Q000235:genetics / Q000502:physiology*
D051550:I-kappa B Kinase