Evidence map›Paper›PMID 21860411›Full record

ArticleOncogene2012

Molecular chaperone complexes with antagonizing activities regulate stability and activity of the tumor suppressor LKB1.

H Gaude, N Aznar, A Delay, A Bres, K Buchet-Poyau, C Caillat, A Vigouroux, C Rogon, A Woods, J-M Vanacker and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 9 institutions in 3 countries.

H GaudeCentre de Recherche en Cancérologie de Lyon, INSERM U1052/CNRS UMR 5286, Lyon, France.
N Aznar
A Delay
A Bres
K Buchet-Poyau
C Caillat
A Vigouroux
C Rogon
A Woods
J-M Vanacker
J Höhfeld
C Perret
P Meyer
M Billaud
C Forcet
Centre National de la Recherche Scientifique · FRLaboratoire d'Enzymologie et Biochimie Structurales · FRCentre de Recherche en Cancérologie de Lyon · FRUniversity of Bonn · DEImperial College London · GBInserm · FRInstitut de Génomique Fonctionnelle de Lyon · FRInstitut pour l'avancée des biosciences · FRUniversité Claude Bernard Lyon 1 · FR

Funding

Medical Research Council
6 · The paper itself

Abstract

LKB1 is a tumor suppressor that is constitutionally mutated in a cancer-prone condition, called Peutz-Jeghers syndrome, as well as somatically inactivated in a sizeable fraction of lung and cervical neoplasms. The LKB1 gene encodes a serine/threonine kinase that associates with the pseudokinase STRAD (STE-20-related pseudokinase) and the scaffolding protein MO25, the formation of this heterotrimeric complex promotes allosteric activation of LKB1. We have previously reported that the molecular chaperone heat shock protein 90 (Hsp90) binds to and stabilizes LKB1. Combining pharmacological studies and RNA interference approaches, we now provide evidence that the co-chaperone Cdc37 participates to the regulation of LKB1 stability. It is known that the Hsp90-Cdc37 complex recognizes a surface within the N-terminal catalytic lobe of client protein kinases. In agreement with this finding, we found that the chaperones Hsp90 and Cdc37 interact with an LKB1 isoform that differs in the C-terminal region, but not with a novel LKB1 variant that lacks a portion of the kinase N-terminal lobe domain. Reconstitution of the two complexes LKB1-STRAD and LKB1-Hsp90-Cdc37 with recombinant proteins revealed that the former is catalytically active whereas the latter is inactive. Furthermore, consistent with a documented repressor function of Hsp90, LKB1 kinase activity was transiently stimulated upon dissociation of Hsp90. Finally, disruption of the LKB1-Hsp90 complex favors the recruitment of both Hsp/Hsc70 and the U-box dependent E3 ubiquitin ligase CHIP (carboxyl terminus of Hsc70-interacting protein) that triggers LKB1 degradation. Taken together, our results establish that the Hsp90-Cdc37 complex controls both the stability and activity of the LKB1 kinase. This study further shows that two chaperone complexes with antagonizing activities, Hsp90-Cdc37 and Hsp/Hsc70-CHIP, finely control the cellular level of LKB1 protein.

Indexed as

AMP-Activated Protein Kinase KinasesCell Cycle ProteinsChaperoninsEnzyme StabilityHSC70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsHumansMolecular ChaperonesMultienzyme ComplexesProtein BindingProtein IsoformsProtein Serine-Threonine KinasesUbiquitin-Protein LigasesAMP-Activated Protein Kinase KinasesCDC37 protein, humanCell Cycle ProteinsChaperoninsHSC70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsMolecular ChaperonesMultienzyme ComplexesProtein IsoformsProtein Serine-Threonine KinasesSTK11 protein, humanSTUB1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID21860411
OpenAlexW2022307344

What OpenQuestion holds

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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.