Evidence map›Paper›PMID 36323257›Full record

ArticleCell reports2022

Disruption of mTORC1 rescues neuronal overgrowth and synapse function dysregulated by Pten loss.

Kamran Tariq, Erin Cullen, Stephanie A Getz, Andie K S Conching, Andrew R Goyette, Mackenzi L Prina, Wei Wang, Meijie Li, Matthew C Weston, Bryan W Luikart

Abstract read
In one paragraph

Article in Cell reports, 2022. 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
–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

38 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. PTEN Subcellular Localization Dictates Function.bioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Article
  10. Cell-Intrinsic Regulation of Epilepsy-Associated Pathology by mTORC1 and mTORC2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

10 authors.

Kamran TariqDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
Erin CullenDepartment of Neurological Sciences, University of Vermont, Burlington, VT 05405, USA.
Stephanie A GetzDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
Andie K S ConchingDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
Andrew R GoyetteDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
Mackenzi L PrinaDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
Wei WangDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
Meijie LiDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
Matthew C WestonDepartment of Neurological Sciences, University of Vermont, Burlington, VT 05405, USA. Electronic address: matthew.c.weston@med.uvm.edu.
Bryan W LuikartDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA. Electronic address: bryan.w.luikart@dartmouth.edu.

Funding

The Impact of PTEN Signaling on Neuronal Form and FunctionR01MH097949 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRYAN W LUIKART · 2012 to 2026
$7.4M
Synaptic changes and hypersynchronous network activity in mTORopathiesR01NS110945 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI WESTON, MATTHEW C · 2019 to 2023
$1.7M
NIMH NIH HHS R01 MH097949NINDS NIH HHS R01 NS110945
6 · The paper itself

Abstract

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a negative regulator of AKT/mTOR signaling pathway. Mutations in PTEN are found in patients with autism, epilepsy, or macrocephaly. In mouse models, Pten loss results in neuronal hypertrophy, hyperexcitability, seizures, and ASD-like behaviors. The underlying molecular mechanisms of these phenotypes are not well delineated. We determined which of the Pten loss-driven aberrations in neuronal form and function are orchestrated by downstream mTOR complex 1 (mTORC1). Rapamycin-mediated inhibition of mTORC1 prevented increase in soma size, migration, spine density, and dendritic overgrowth in Pten knockout dentate gyrus granule neurons. Genetic knockout of Raptor to disrupt mTORC1 complex formation blocked Pten loss-mediated neuronal hypertrophy. Electrophysiological recordings revealed that genetic disruption of mTORC1 rescued Pten loss-mediated increase in excitatory synaptic transmission. We have identified an essential role for mTORC1 in orchestrating Pten loss-driven neuronal hypertrophy and synapse formation.

Indexed as

NeuronsSynapsesAnimalsHypertrophyMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutPTEN PhosphohydrolaseTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1PTEN PhosphohydrolaseTOR Serine-Threonine KinasesautismCP: Cell biologyCP: NeurosciencedendritemTORPTENrapamycinRaptorsynapse

Identifiers

PMID36323257
PMCPMC9743803

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.