Evidence map›Paper›PMID 17000765›Full record

ArticleMolecular and cellular biology2006

The Ral/exocyst effector complex counters c-Jun N-terminal kinase-dependent apoptosis in Drosophila melanogaster.

Maria Balakireva, Carine Rossé, Johanna Langevin, Yu-chen Chien, Michel Gho, Geneviève Gonzy-Treboul, Stéphanie Voegeling-Lemaire, Sandra Aresta, Jean-Antoine Lepesant, Yohanns Bellaiche and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. A signalling cascade for Ral.Small GTPases · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  9. Article
  10. Article
  11. Review
  12. Polarized Exocytosis.Cold Spring Harbor perspectives in biology · 2017
    Review
  13. Article
  14. The Exocyst at a Glance.Journal of cell science · 2015
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

12 authors at 5 institutions in 2 countries.

Maria BalakirevaInstitut Curie, INSERM U528, Groupe d'Analyse des Réseaux de Transduction (ART), 26 rue d'Ulm, 75248 Paris cedex 05, France.
Carine Rossé
Johanna Langevin
Yu-chen Chien
Michel Gho
Geneviève Gonzy-Treboul
Stéphanie Voegeling-Lemaire
Sandra Aresta
Jean-Antoine Lepesant
Yohanns Bellaiche
Michael White
Jacques Camonis
Inserm · FRBiologie cellulaire et Cancer · FRThe University of Texas Southwestern Medical Center · USCentre National de la Recherche Scientifique · FRHybrigenics (France) · FR

Funding

COMPONENTS OF RAS-MEDIATED GROWTH CONTROLR01CA071443 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WHITE, MICHAEL A. · 1996 to 2015
$4.8M
NCI NIH HHS R01 CA071443
6 · The paper itself

Abstract

Ral GTPase activity is a crucial cell-autonomous factor supporting tumor initiation and progression. To decipher pathways impacted by Ral, we have generated null and hypomorph alleles of the Drosophila melanogaster Ral gene. Ral null animals were not viable. Reduced Ral expression in cells of the sensory organ lineage had no effect on cell division but led to postmitotic cell-specific apoptosis. Genetic epistasis and immunofluorescence in differentiating sensory organs suggested that Ral activity suppresses c-Jun N-terminal kinase (JNK) activation and induces p38 mitogen-activated protein (MAP) kinase activation. HPK1/GCK-like kinase (HGK), a MAP kinase kinase kinase kinase that can drive JNK activation, was found as an exocyst-associated protein in vivo. The exocyst is a Ral effector, and the epistasis between mutants of Ral and of msn, the fly ortholog of HGK, suggest the functional relevance of an exocyst/HGK interaction. Genetic analysis also showed that the exocyst is required for the execution of Ral function in apoptosis. We conclude that in Drosophila Ral counters apoptotic programs to support cell fate determination by acting as a negative regulator of JNK activity and a positive activator of p38 MAP kinase. We propose that the exocyst complex is Ral executioner in the JNK pathway and that a cascade from Ral to the exocyst to HGK would be a molecular basis of Ral action on JNK.

Indexed as

ApoptosisAllelesAnimalsCell DifferentiationCell LineageDrosophila melanogasterEmbryo, NonmammalianEnzyme ActivationEpistasis, GeneticGene DeletionGene Expression Regulation, DevelopmentalGenes, EssentialGenes, InsectGTP-Binding ProteinsImmunohistochemistryMAP Kinase Kinase 4GTP-Binding Proteinshematopoietic progenitor kinase 1MAP Kinase Kinase 4Mitogen-Activated Protein Kinase 9p38 Mitogen-Activated Protein KinasesProtein Serine-Threonine Kinases

Identifiers

PMID17000765
PMCPMC1636832
OpenAlexW2126960848

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.