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. 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 language | English |
|---|---|
| Pages (from-to) | 189-191 |
| Number of pages | 3 |
| Journal | Autophagy |
| Volume | 6 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 1 2010 |
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Keywords
- AMPK
- JNK1
- mTOR
- Nutrient deprivation
- Rapamycin
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
Cite this
IKK connects autophagy to major stress pathways. / Criollo, Alfredo; Senovilla, Laura; Authier, Hélène; Maiuri, Maria Chiara; Morselli, Eugenia; Vitale, Ilio; Kepp, Oliver; Tasdemir, Ezgi; Galluzzi, Lorenzo; Shen, Si; Tailler, Maximilien; Delahaye, Nicolas; Tesniere, Antoine; De Stefano, Daniela; Younes, Aména Ben; Harper, Francis; Pierron, Gérard; Lavandero, Sergio; Zitvoge, Laurence; Israel, Alain; Baud, Véronique; Kroemer, Guido.
In: Autophagy, Vol. 6, No. 1, 01.01.2010, p. 189-191.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - IKK connects autophagy to major stress pathways
AU - Criollo, Alfredo
AU - Senovilla, Laura
AU - Authier, Hélène
AU - Maiuri, Maria Chiara
AU - Morselli, Eugenia
AU - Vitale, Ilio
AU - Kepp, Oliver
AU - Tasdemir, Ezgi
AU - Galluzzi, Lorenzo
AU - Shen, Si
AU - Tailler, Maximilien
AU - Delahaye, Nicolas
AU - Tesniere, Antoine
AU - De Stefano, Daniela
AU - Younes, Aména Ben
AU - Harper, Francis
AU - Pierron, Gérard
AU - Lavandero, Sergio
AU - Zitvoge, Laurence
AU - Israel, Alain
AU - Baud, Véronique
AU - Kroemer, Guido
PY - 2010/1/1
Y1 - 2010/1/1
N2 - 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.
AB - 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.
KW - AMPK
KW - JNK1
KW - mTOR
KW - Nutrient deprivation
KW - Rapamycin
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UR - http://www.scopus.com/inward/citedby.url?scp=75149129642&partnerID=8YFLogxK
U2 - 10.4161/auto.6.1.10818
DO - 10.4161/auto.6.1.10818
M3 - Article
C2 - 20110771
AN - SCOPUS:75149129642
VL - 6
SP - 189
EP - 191
JO - Autophagy
JF - Autophagy
SN - 1554-8627
IS - 1
ER -