Evidence map›Paper›PMID 17308101›Full record

ArticleCancer research2007

TSC1 sets the rate of ribosome export and protein synthesis through nucleophosmin translation.

Corey L Pelletier, Leonard B Maggi, Suzanne N Brady, Danielle K Scheidenhelm, David H Gutmann, Jason D Weber

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Deconvoluting mTOR biology.Cell cycle (Georgetown, Tex.) · 2012
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Targeting of eEF1A with Amaryllidaceae isocarbostyrils as a strategy to combat melanomas.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010
    Article
  17. Article
  18. Review
  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

6 authors at 3 institutions in 1 country.

Corey L PelletierDivision of Molecular Oncology, Department of Internal Medicine, Siteman Cancer Center, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Leonard B Maggi
Suzanne N Brady
Danielle K Scheidenhelm
David H Gutmann
Jason D Weber
Molecular Oncology (United States) · USNeurology, Inc · USWashington University in St. Louis · US

Funding

NATIONAL RESEARCH SERVICE AWARD-MEDICAL SCIENTISTT32GM007200 · NIGMS · WASHINGTON UNIVERSITY · PI YOKOYAMA, WAYNE M. · 1985 to 2024
$59.8M
PRECLINICAL MOUSE: CENTRAL NERVOUS SYSTEM CANCERSU01CA084314 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI VAN DYKE, TERRY A · 1999 to 2009
$9.2M
Characterization of p53-independent ARF pathwayR01GM066032 · NIGMS · WASHINGTON UNIVERSITY · PI WEBER, JASON · 2003 to 2007
$1.3M
NCI NIH HHS U01 CA084314NCI NIH HHS U01 CA 84314NIGMS NIH HHS 5T32 GM 07200NIGMS NIH HHS GM 066032NIGMS NIH HHS R01 GM066032NIGMS NIH HHS T32 GM007200
6 · The paper itself

Abstract

Nucleophosmin (B23) is a nucleolar phosphoprotein that has been implicated in numerous cellular processes. In particular, nucleophosmin interacts with nucleolar components of newly synthesized ribosomes to promote ribosome nuclear export. Nucleophosmin is a classic mitogen-induced protein, with changes in its expression correlating with growth factor stimulation. In this study, we examined the underlying mechanism of nucleophosmin induction and showed that hyperproliferative signals emanating from oncogenic H-Ras(V12) cause tremendous increases in nucleophosmin protein expression. Nucleophosmin protein accumulation was dependent on mammalian target of rapamycin (mTOR) activation, as rapamycin completely prevented nucleophosmin induction. Consistent with this finding, genetic ablation of Tsc1, a major upstream inhibitor of mTOR, resulted in nucleophosmin protein induction through increased translation of existing nucleophosmin mRNAs. Increases in nucleophosmin protein accumulation were suppressed by reintroduction of TSC1. Induction of nucleophosmin through Tsc1 loss resulted in a greater pool of actively translating ribosomes in the cytoplasm, higher overall rates of protein synthesis, and increased cell proliferation, all of which were dependent on efficient nucleophosmin nuclear export. Nucleophosmin protein accumulation in the absence of Tsc1 promoted the nuclear export of maturing ribosome subunits, providing a mechanistic link between TSC1/mTOR signaling, nucleophosmin-mediated nuclear export of ribosome subunits, protein synthesis levels, and cell growth.

Indexed as

AnimalsChromonesHumansMiceMorpholinesNuclear ProteinsNucleophosminPlatelet-Derived Growth FactorProtein BiosynthesisProtein Kinasesras ProteinsRibosomesRNA, MessengerSirolimusTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 Protein2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesMorpholinesMTOR protein, humanmTOR protein, mouseNPM1 protein, humanNpm1 protein, mouseNuclear ProteinsNucleophosminPlatelet-Derived Growth FactorProtein Kinasesras ProteinsRNA, MessengerSirolimusTOR Serine-Threonine KinasesTSC1 protein, humanTsc1 protein, mouseTuberous Sclerosis Complex 1 ProteinTumor Suppressor Proteins

Identifiers

PMID17308101
PMCPMC2859708
OpenAlexW2151409808

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.