Evidence map›Paper›PMID 11390358›Full record

ArticleGenes & development2001

TSC1 and TSC2 tumor suppressors antagonize insulin signaling in cell growth.

X Gao, D Pan

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

193 citing papers in PubMed, 3 syntheses or guidelines pooled it, 458 citations in OpenAlex.

  1. Rapamycin and rapalogs for tuberous sclerosis complex.The Cochrane database of systematic reviews · 2023
    Pooled it
  2. Rapamycin and rapalogs for tuberous sclerosis complex.The Cochrane database of systematic reviews · 2016
    Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Review
  7. Gene model for the ortholog ofmicroPublication biology · 2026
    Article
  8. Review
  9. Article
  10. Gene model for the ortholog ofmicroPublication biology · 2025
    Article
  11. Unveiling the Tumor Suppressors: Insights from Drosophila.Advances in experimental medicine and biology · 2025
    Review
  12. AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024
    Review
  13. Review
  14. Article
  15. Review
  16. UsingCells · 2023
    Review
  17. Article
  18. Article
  19. Review
  20. International journal of molecular sciences · 2022
    Review

133 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

2 authors at 1 institution in 1 country.

X GaoDepartment of Physiology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9040, USA.
D Pan
The University of Texas Southwestern Medical Center · US

Funding

SIZE-CONTROL MECHANISMS IN DROSOPHILA DEVELOPMENTR01GM062323 · NIGMS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI PAN, DUOJIA · 2001 to 2005
$1.4M
NIGMS NIH HHS GM62323NIGMS NIH HHS R01 GM062323
6 · The paper itself

Abstract

Tuberous sclerosis is a human disease caused by mutations in the TSC1 or the TSC2 tumor suppressor gene. Previous studies of a Drosophila TSC2 homolog suggested a role for the TSC genes in maintaining DNA content, with loss of TSC2 leading to polyploidy and increased cell size. We have isolated mutations in the Drosophila homolog of the TSC1 gene. We show that TSC1 and TSC2 form a complex and function in a common pathway to control cellular growth. Unlike previous studies, our work shows that TSC1(-) or TSC2(-) cells are diploid. We find that, strikingly, the heterozygosity of TSC1 or TSC2 is sufficient to rescue the lethality of loss-of-function insulin receptor mutants. Further genetic analyses suggest that the TSC genes act in a parallel pathway that converges on the insulin pathway downstream from Akt. Taken together, our studies identified the TSC tumor suppressors as novel negative regulators of insulin signaling.

Indexed as

Genes, Tumor SuppressorProtein Serine-Threonine KinasesSignal TransductionAnimalsCell DivisionCell SizeDiploidyDrosophilaDrosophila ProteinsFlow CytometryInsulinLoss of HeterozygosityMutationPolymerase Chain ReactionPrecipitin TestsProteinsAkt1 protein, DrosophilaDrosophila ProteinsInsulinProteinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor, InsulinRepressor ProteinsTSC1 protein, humanTSC2 protein, humanTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID11390358
PMCPMC312704
OpenAlexW2103304405

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.