Evidence map›Paper›PMID 12214276›Full record

ArticleOncogene2002

Rheb is in a high activation state and inhibits B-Raf kinase in mammalian cells.

Edward Im, Friederike C von Lintig, Jeffrey Chen, Shunhui Zhuang, Wansong Qui, Shoaib Chowdhury, Paul F Worley, Gerry R Boss, Renate B Pilz

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 130 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Regulation of the Small GTPase Ras and Its Relevance to Human Disease.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  7. Review
  8. Review
  9. Review
  10. Non-canonical Raf-1/p70S6K signalling in non-small-cell lung cancer.Journal of cellular and molecular medicine · 2019
    Article
  11. Review
  12. Article
  13. Article
  14. Analysis of TSC1 mutation spectrum in mucosal melanoma.Journal of cancer research and clinical oncology · 2018
    Article
  15. Article
  16. Article
  17. 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
  18. mTORC1 signaling in primary central nervous system lymphoma.Surgical neurology international · 2016
    Article
  19. Regulation of RAF protein kinases in ERK signalling.Nature reviews. Molecular cell biology · 2015
    Review
  20. Article

1 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

9 authors at 2 institutions in 1 country.

Edward ImDepartment of Medicine and Cancer Center, University of California, San Diego, La Jolla, California, CA 92093-0652, USA.
Friederike C von Lintig
Jeffrey Chen
Shunhui Zhuang
Wansong Qui
Shoaib Chowdhury
Paul F Worley
Gerry R Boss
Renate B Pilz
University of California, San Diego · USJohns Hopkins University · US

Funding

REGULATION OF GENE EXPRESSION BY NO/CGMPR01GM055586 · NIGMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI PILZ, RENATE B · 1998 to 2002
$707k
MEASUREMENT OF RAS ACTIVATION IN LUNG CANCERR21CA081115 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI BOSS, GERRY R · 1999 to 2000
$114k
DEVELOPMENT OF AN AUTOMATED RAS MEASUREMENT DEVICER21CA076968 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI BOSS, GERRY R · 1997 to 1999
–
NCI NIH HHS CA76968NCI NIH HHS CA81115NIGMS NIH HHS GM55586NIMH NIH HHS MH53608
6 · The paper itself

Abstract

Rheb (Ras homolog enriched in brain) is a member of the Ras family of proteins, and is in the immediate Ras/Rap/Ral subfamily. We found in three different mammalian cell lines that Rheb was highly activated, to levels much higher than for Ras or Rap 1, and that Rheb's activation state was unaffected by changes in growth conditions. Rheb's high activation was not secondary to unique glycine to arginine, or glycine to serine substitutions at positions 14 and 15, corresponding to Ras residues 12 and 13, since Rheb R14G and R14G, S15G mutants had similarly high activation levels as wild type Rheb. These data are consistent with earlier work which showed that purified Rheb has similar GTPase activity as Ras, and suggest a relative intracellular deficiency of Rheb GTPase activating proteins (GAPs) compared to Rheb activators. Further evidence for relatively low intracellular GAP activity was that increased Rheb expression led to a marked increase in Rheb activation. Rheb, like Ras and Rap1, bound B-Raf kinase, but in contrast to Ras and Rap 1, Rheb inhibited B-Raf kinase activity and prevented B-Raf-dependent activation of the transcription factor Elk-1. Thus, Rheb appears to be a unique member of the Ras/Rap/Ral subfamily, and in mammalian systems may serve to regulate B-Raf kinase activity.

Indexed as

AnimalsCHO CellsCricetinaeGene Expression RegulationMAP Kinase Signaling SystemMonomeric GTP-Binding ProteinsMutagenesis, Site-DirectedNeuropeptidesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafSignal TransductionSpecies SpecificityTransfectionBraf protein, ratMonomeric GTP-Binding ProteinsNeuropeptidesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-raf

Identifiers

PMID12214276
OpenAlexW2044247583

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.