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 Israel; Véronique Baud; Guido Kroemer

doi:10.4161/auto.6.1.10818

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 journal › Article › peer-review

39 Citations (Scopus)

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	https://doi.org/10.4161/auto.6.1.10818
Publication status	Published - 1 Jan 2010

Keywords

AMPK
JNK1
Nutrient deprivation
Rapamycin
mTOR

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Criollo, A., Senovilla, L., Authier, H., Maiuri, M. C., Morselli, E., Vitale, I., Kepp, O., Tasdemir, E., Galluzzi, L., Shen, S., Tailler, M., Delahaye, N., Tesniere, A., De Stefano, D., Younes, A. B., Harper, F., Pierron, G., Lavandero, S., Zitvoge, L., ... Kroemer, G. (2010). IKK connects autophagy to major stress pathways. Autophagy, 6(1), 189-191. https://doi.org/10.4161/auto.6.1.10818

@article{fce89eb00e7f4538871e3ef4df70e013,

title = "IKK connects autophagy to major stress pathways",

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.",

keywords = "AMPK, JNK1, Nutrient deprivation, Rapamycin, mTOR",

author = "Alfredo Criollo and Laura Senovilla and H{\'e}l{\`e}ne Authier and Maiuri, {Maria Chiara} and Eugenia Morselli and Ilio Vitale and Oliver Kepp and Ezgi Tasdemir and Lorenzo Galluzzi and Si Shen and Maximilien Tailler and Nicolas Delahaye and Antoine Tesniere and {De Stefano}, Daniela and Younes, {Am{\'e}na Ben} and Francis Harper and G{\'e}rard Pierron and Sergio Lavandero and Laurence Zitvoge and Alain Israel and V{\'e}ronique Baud and Guido Kroemer",

note = "Funding Information: G.K. is supported by the Ligue Nationale contre le Cancer, ANR, Canc{\'e}rop{\^o}le Ile-de-France, Institut National du Cancer, European Commission (Active p53, Apo-Sys, RIGHT, ChemoRes, ApopTrain), and FRM. We thank the International Collaboration Program ECOS-CONICYT, grant C08S01 (to G.K. and S.L.). V.B. is supported by Agence Nationale pour la Recherche, Association pour la Recherche sur le Cancer, Belgian InterUniversity Attraction Pole, Canc{\'e}ropole Ile-de-France, INCa and Universit{\'e} Paris Descartes.",

year = "2010",

month = jan,

day = "1",

doi = "10.4161/auto.6.1.10818",

language = "English",

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journal = "Autophagy",

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Criollo, A, Senovilla, L, Authier, H, Maiuri, MC, Morselli, E, Vitale, I, Kepp, O, Tasdemir, E, Galluzzi, L, Shen, S, Tailler, M, Delahaye, N, Tesniere, A, De Stefano, D, Younes, AB, Harper, F, Pierron, G, Lavandero, S, Zitvoge, L, Israel, A, Baud, V & Kroemer, G 2010, 'IKK connects autophagy to major stress pathways', Autophagy, vol. 6, no. 1, pp. 189-191. https://doi.org/10.4161/auto.6.1.10818

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

N1 - Funding Information: G.K. is supported by the Ligue Nationale contre le Cancer, ANR, Cancéropôle Ile-de-France, Institut National du Cancer, European Commission (Active p53, Apo-Sys, RIGHT, ChemoRes, ApopTrain), and FRM. We thank the International Collaboration Program ECOS-CONICYT, grant C08S01 (to G.K. and S.L.). V.B. is supported by Agence Nationale pour la Recherche, Association pour la Recherche sur le Cancer, Belgian InterUniversity Attraction Pole, Cancéropole Ile-de-France, INCa and Université Paris Descartes.

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 - Nutrient deprivation

KW - Rapamycin

KW - mTOR

UR - http://www.scopus.com/inward/record.url?scp=75149129642&partnerID=8YFLogxK

U2 - 10.4161/auto.6.1.10818

DO - 10.4161/auto.6.1.10818

M3 - Article

AN - SCOPUS:75149129642

SN - 1554-8627

VL - 6

SP - 189

EP - 191

JO - Autophagy

JF - Autophagy

IS - 1

ER -

IKK connects autophagy to major stress pathways

Abstract

Keywords

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