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

Universidad de Chile

Producción científica › revisión exhaustiva

39 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	189-191
Número de páginas	3
Publicación	Autophagy
Volumen	6
N.º	1
DOI	https://doi.org/10.4161/auto.6.1.10818
Estado	Published - ene. 1 2010

Financiación

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.

Financiadores	Número del financiador
Belgian InterUniversity Attraction Pole, Cancéropole Ile-de-France
Cancéropôle Ile-de-France
ChemoRes
International Collaboration Program ECOS-CONICYT	C08S01
Association pour la Recherche sur le Cancer
European Commission
Agence Nationale de la Recherche
Fondation pour la Recherche Médicale
Ligue Contre le Cancer
Université Paris Descartes
Institut National Du Cancer
Right to Care

ASJC Scopus Subject Areas

Molecular Biology
Cell Biology

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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

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, n.º 1, pp. 189-191. https://doi.org/10.4161/auto.6.1.10818

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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.",

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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.",

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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.

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IKK connects autophagy to major stress pathways

Resumen

Financiación

ASJC Scopus Subject Areas

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