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
IKK connects autophagy to major stress pathways. / Criollo, Alfredo; Senovilla, Laura; Authier, Hélène et al.
In:
Autophagy, Vol. 6, No. 1, 01.01.2010, p. 189-191.
Research output: Contribution to journal › Article › peer-review
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
Criollo A, Senovilla L, Authier H, Maiuri MC, Morselli E, Vitale I et al. IKK connects autophagy to major stress pathways. Autophagy. 2010 Jan 1;6(1):189-191. doi: 10.4161/auto.6.1.10818
Criollo, Alfredo ; Senovilla, Laura ; Authier, Hélène et al. / IKK connects autophagy to major stress pathways. In: Autophagy. 2010 ; Vol. 6, No. 1. pp. 189-191.
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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.",
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",
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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.
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