Evidence map›Paper›PMID 38212374›Full record

ReviewMolecular psychiatry2024

The role of TSC1 and TSC2 proteins in neuronal axons.

Vasiliki Karalis, Delaney Wood, Nicole A Teaney, Mustafa Sahin

Abstract readReview
In one paragraph

Review in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. TSC2 is a stress granule suppressor.bioRxiv : the preprint server for biology · 2026
    Article
  4. Tuberous sclerosis complex.Nature reviews. Disease primers · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Oncogenic activation ofGenes & diseases · 2025
    Review
  9. The Development of Methods of BLOTCHIPCurrent issues in molecular biology · 2025
    Review
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

4 authors at 1 institution in 1 country.

Vasiliki KaralisRosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Delaney WoodFM Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA, 02115, USA.
Nicole A TeaneyRosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Mustafa SahinRosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA. Mustafa.sahin@childrens.harvard.edu.ORCID 0000-0001-7044-2953
Boston Children's Hospital · US

Funding

Genetic Analysis and Manipulation Core (GAEC)P50HD105351 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI SCOTT Loren POMEROY, MUSTAFA SAHIN · 2021 to 2026
$9.4M
Supplement request for Training GrantT32NS007473 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI Elizabeth C. Engle, Thomas L. Schwarz · 1999 to 2026
$6.9M
Disrupted ciliary signaling in the brain pathology of Tuberous Sclerosis Complex (Diversity Supplement)R01NS113591 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI SAHIN, MUSTAFA · 2019 to 2022
$2.9M
NICHD NIH HHS P50 HD105351NINDS NIH HHS R01 NS113591NINDS NIH HHS T32 NS007473U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) R01NS113591
6 · The paper itself

Abstract

Tuberous Sclerosis Complex 1 and 2 proteins, TSC1 and TSC2 respectively, participate in a multiprotein complex with a crucial role for the proper development and function of the nervous system. This complex primarily acts as an inhibitor of the mechanistic target of rapamycin (mTOR) kinase, and mutations in either TSC1 or TSC2 cause a neurodevelopmental disorder called Tuberous Sclerosis Complex (TSC). Neurological manifestations of TSC include brain lesions, epilepsy, autism, and intellectual disability. On the cellular level, the TSC/mTOR signaling axis regulates multiple anabolic and catabolic processes, but it is not clear how these processes contribute to specific neurologic phenotypes. Hence, several studies have aimed to elucidate the role of this signaling pathway in neurons. Of particular interest are axons, as axonal defects are associated with severe neurocognitive impairments. Here, we review findings regarding the role of the TSC1/2 protein complex in axons. Specifically, we will discuss how TSC1/2 canonical and non-canonical functions contribute to the formation and integrity of axonal structure and function.

Indexed as

AxonsNeuronsTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinAnimalsHumansMutationSignal TransductionTOR Serine-Threonine KinasesTuberous SclerosisTumor Suppressor ProteinsTOR Serine-Threonine KinasesTSC1 protein, humanTSC2 protein, humanTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID38212374
PMCPMC12863650
OpenAlexW4390748434

What OpenQuestion holds

Textmetadata
LicenceTDM
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.