Evidence map›Paper›PMID 18521078›Full record

ArticleOncogene2008

Constitutively active Rheb induces oncogenic transformation.

H Jiang, P K Vogt

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. The mTOR pathway controls phosphorylation of BRAF at T401.Cell communication and signaling : CCS · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. The Lysosome Signaling Platform: Adapting With the Times.Frontiers in cell and developmental biology · 2019
    Review
  13. Review
  14. Article
  15. Influence of miR-155 on Cell Apoptosis in Rats with Ischemic Stroke: Role of the Ras Homolog Enriched in Brain (Rheb)/mTOR Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  16. Review
  17. Article
  18. RHEB1 expression in embryonic and postnatal mouse.Histochemistry and cell biology · 2016
    Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

H Jiang1Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA. hjiang@scripps.edu
P K Vogt
Scripps Research Institute · US

Funding

Small Molecules and Targeted Gene Delivery in Tumor AngiogenesisP01CA078045 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI VOGT, PETER K · 1998 to 2008
$10.2M
P3K, RETROVIRAL ONCOGENE AND HOMOLOG OF PI 3-KINASER01CA078230 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI VOGT, PETER K · 1998 to 2013
$5.6M
Controlling the Max NetworkR01CA107094 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI VOGT, PETER K · 2004 to 2008
$1.2M
NCI NIH HHS P01 CA078045NCI NIH HHS R01 CA078230NCI NIH HHS R01 CA107094
6 · The paper itself

Abstract

Rheb (Ras-homolog enriched in brain) is a component of the phosphatidylinositol 3-kinase (PI3K) target of rapamycin (TOR) signaling pathway, functioning as a positive regulator of TOR. Constitutively active mutants of Rheb induce oncogenic transformation in cell culture. The transformed cells are larger and contain more protein than their normal counterparts. They show constitutive phosphorylation of the ribosomal protein S6 kinase and the eukaryotic initiation factor 4E-binding protein 1, two downstream targets of TOR. The TOR-specific inhibitor rapamycin strongly interferes with transformation induced by constitutively active Rheb, suggesting that TOR activity is essential for the oncogenic effects of mutant Rheb. Rheb-induced transformation is also dependent on a C-terminal farnesylation signal that mediates localization to a cellular membrane. An engineered N-terminal myristylation signal can substitute for the farnesylation. Immunofluorescence localizes wild-type and mutant Rheb to vesicular structures in the cytoplasm, overlapping with the endoplasmic reticulum.

Indexed as

Cell Transformation, NeoplasticAnimalsCells, CulturedChick EmbryoDNA-Binding ProteinsForkhead Box Protein O1Forkhead Transcription FactorsGuanosine TriphosphateHumansMonomeric GTP-Binding ProteinsNeuropeptidesNuclear ProteinsPhosphatidylinositol 3-KinasesPrenylationProtein KinasesRas Homolog Enriched in Brain ProteinDNA-Binding ProteinsForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanGuanosine TriphosphateMonomeric GTP-Binding ProteinsMTOR protein, humanNeuropeptidesNuclear ProteinsPhosphatidylinositol 3-KinasesProtein KinasesRas Homolog Enriched in Brain ProteinRHEB protein, humanTOR Serine-Threonine KinasesY-Box-Binding Protein 1YBX1 protein, human

Identifiers

PMID18521078
PMCPMC2562864
OpenAlexW2056739666

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.