Evidence map›Paper›PMID 19959994›Full record

ArticleThe EMBO journal2010

The IKK complex contributes to the induction of autophagy.

Alfredo Criollo, Laura Senovilla, Hélène Authier, Maria Chiara Maiuri, Eugenia Morselli, Ilio Vitale, Oliver Kepp, Ezgi Tasdemir, Lorenzo Galluzzi, Shensi Shen and 12 more

Abstract read
In one paragraph

Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 2 pooled it
17.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

180 citing papers in PubMed, 2 syntheses or guidelines pooled it, 292 citations in OpenAlex.

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  13. The helicase-like transcription factor redirects the autophagic flux and restricts human T cell leukemia virus type 1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
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120 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 10 institutions in 3 countries.

Alfredo CriolloINSERM, U848, Villejuif, France.
Laura Senovilla
Hélène Authier
Maria Chiara Maiuri
Eugenia Morselli
Ilio Vitale
Oliver Kepp
Ezgi Tasdemir
Lorenzo Galluzzi
Shensi Shen
Maximilien Tailler
Nicolas Delahaye
Antoine Tesniere
Daniela De Stefano
Aména Ben Younes
Francis Harper
Gérard Pierron
Sergio Lavandero
Laurence Zitvogel
Alain Israel
Véronique Baud
Guido Kroemer
Université Paris-Saclay · FRInstitut Gustave Roussy · FRUniversité Paris-Sud · FRCentre National de la Recherche Scientifique · FRInserm · FRUniversity of Chile · CLInstitut Cochin · FRInstitut Pasteur · FRUniversité Paris Cité · FRUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In response to stress, cells start transcriptional and transcription-independent programs that can lead to adaptation or death. Here, we show that multiple inducers of autophagy, including nutrient depletion, trigger the activation of the IKK (IkappaB kinase) complex that is best known for its essential role in the activation of the transcription factor NF-kappaB by stress. Constitutively active IKK subunits stimulated autophagy and transduced multiple signals that operate in starvation-induced autophagy, including the phosphorylation of AMPK and JNK1. Genetic inhibition of the nuclear translocation of NF-kappaB or ablation of the p65/RelA NF-kappaB subunit failed to suppress IKK-induced autophagy, indicating that IKK can promote the autophagic pathway in an NF-kappaB-independent manner. In murine and human cells, knockout and/or knockdown of IKK subunits (but not that of p65) prevented the induction of autophagy in response to multiple stimuli. Moreover, the knockout of IKK-beta suppressed the activation of autophagy by food deprivation or rapamycin injections in vivo, in mice. Altogether, these results indicate that IKK has a cardinal role in the stimulation of autophagy by physiological and pharmacological stimuli.

Indexed as

AnimalsAutophagyCells, CulturedHeLa CellsHumansI-kappa B KinaseMiceMice, Inbred C57BLMice, TransgenicMultiprotein ComplexesNF-kappa BNIH 3T3 CellsSignal TransductionI-kappa B KinaseMultiprotein ComplexesNF-kappa B

Identifiers

PMID19959994
PMCPMC2830700
OpenAlexW1974251566

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.