Evidence map›Paper›PMID 16894031›Full record

ArticleMolecular and cellular biology2006

mTOR-independent translational control of the extrinsic cell death pathway by RalA.

Amith Panner, Jean L Nakamura, Andrew T Parsa, Pablo Rodriguez-Viciana, Mitchel S Berger, David Stokoe, Russell O Pieper

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Roles of c-FLIP in Apoptosis, Necroptosis, and Autophagy.Journal of carcinogenesis & mutagenesis · 2013
    Article
  4. c-FLIP, a master anti-apoptotic regulator.Experimental oncology · 2012
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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

7 authors at 3 institutions in 2 countries.

Amith PannerUCSF Cancer Center, 2340 Sutter St., Rm N219, San Francisco, CA 94115-0875, USA.
Jean L Nakamura
Andrew T Parsa
Pablo Rodriguez-Viciana
Mitchel S Berger
David Stokoe
Russell O Pieper
UCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of California, San Francisco · USPediatric Brain Tumor Foundation · US

Funding

Tissue CoreP50CA097257 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joseph F Costello · 2002 to 2026
$57.4M
Contributions of Akt to Glioblastoma FormationR01CA094989 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PIEPER, RUSSELL O · 2002 to 2006
$1.7M
UNDERSTANDING TRAIL SENSITIVITY IN HUMAN GLIOMAR01CA115638 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PIEPER, RUSSELL O. · 2006 to 2010
$1.2M
NCI NIH HHS P50 CA097257NCI NIH HHS P50 CA97257NCI NIH HHS R01 CA094989NCI NIH HHS R01 CA115638NCI NIH HHS R01 CA94989
6 · The paper itself

Abstract

Oncogenic potential is associated with translational regulation, and the prevailing view is that oncogenes use mTOR-dependent pathways to up-regulate the synthesis of proteins critical for transformation. In this study, we show that RalA, a key mediator of Ras transformation, is also linked to the translational machinery. At least part of this linkage, however, is independent of mTOR and acts through RalBP1 to suppress cdc42-mediated activation of S6 kinase and the translation of the antiapoptotic protein FLIP(S). This action, rather than contributing to transformation, opens a latent tumor-suppressive mechanism that can be activated by tumor necrosis factor-related apoptosis-inducing ligand. These results show that the translational machinery is linked to tumor suppression as well as cell-proliferative pathways and that the reestablishment of cell death pathways by activation of the Ral oncogenic program provides a means for selective therapeutic targeting of Ral-driven malignancies.

Indexed as

Protein BiosynthesisAnimalsApoptosis Regulatory ProteinsAstrocytesATP-Binding Cassette TransportersCASP8 and FADD-Like Apoptosis Regulating Proteincdc42 GTP-Binding ProteinCell DeathCell LineGene Expression RegulationHumansIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMicePhosphorylationProtein BindingApoptosis Regulatory ProteinsATP-Binding Cassette TransportersCASP8 and FADD-Like Apoptosis Regulating Proteincdc42 GTP-Binding ProteinCFLAR protein, humanCflar protein, mouseIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMTOR protein, humanmTOR protein, mouseProtein Kinasesral GTP-Binding ProteinsRibosomal Protein S6 KinasesTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTnfsf10 protein, mouseTOR Serine-Threonine KinasesTumor Necrosis Factor-alpha

Identifiers

PMID16894031
PMCPMC1636864
OpenAlexW2148455395

What Socratic 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 Socratic graph.