Evidence map›Paper›PMID 29476105›Full record

ArticleScientific reports2018

mTOR-dependent alterations of Kv1.1 subunit expression in the neuronal subset-specific Pten knockout mouse model of cortical dysplasia with epilepsy.

Lena H Nguyen, Anne E Anderson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Anti-seizure gene therapy for focal cortical dysplasia.Brain : a journal of neurology · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. mTOR Modulation ofInternational journal of molecular sciences · 2022
    Article
  13. Immunity, Ion Channels and Epilepsy.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  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

2 authors at 2 institutions in 1 country.

Lena H NguyenDepartment of Neuroscience, Baylor College of Medicine, Houston, TX, USA.
Anne E AndersonDepartment of Neuroscience, Baylor College of Medicine, Houston, TX, USA. annea@bcm.edu.
Baylor College of Medicine · USTexas Children's Hospital · US

Funding

Steps towards a paternal gene activation therapy for Angelman syndromeU54HD083092 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI NELSON, DAVID LOREN, NEUL, JEFFREY L · 2014 to 2019
$7.8M
Signaling pathway dysregulation in epilepsyR01NS081053 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ANDERSON, ANNE E · 2013 to 2016
$1.4M
NICHD NIH HHS U54 HD083092NINDS NIH HHS R01 NS081053
6 · The paper itself

Abstract

Cortical dysplasia (CD) is a common cause for intractable epilepsy. Hyperactivation of the mechanistic target of rapamycin (mTOR) pathway has been implicated in CD; however, the mechanisms by which mTOR hyperactivation contribute to the epilepsy phenotype remain elusive. Here, we investigated whether constitutive mTOR hyperactivation in the hippocampus is associated with altered voltage-gated ion channel expression in the neuronal subset-specific Pten knockout (NS-Pten KO) mouse model of CD with epilepsy. We found that the protein levels of Kv1.1, but not Kv1.2, Kv1.4, or Kvβ2, potassium channel subunits were increased, along with altered Kv1.1 distribution, within the hippocampus of NS-Pten KO mice. The aberrant Kv1.1 protein levels were present in young adult (≥postnatal week 6) but not juvenile (≤postnatal week 4) NS-Pten KO mice. No changes in hippocampal Kv1.1 mRNA levels were found between NS-Pten KO and WT mice. Interestingly, mTOR inhibition with rapamycin treatment at early and late stages of the pathology normalized Kv1.1 protein levels in NS-Pten KO mice to WT levels. Together, these studies demonstrate altered Kv1.1 protein expression in association with mTOR hyperactivation in NS-Pten KO mice and suggest a role for mTOR signaling in the modulation of voltage-gated ion channel expression in this model.

Indexed as

AnimalsDisease Models, AnimalEpilepsyGene Expression RegulationHippocampusHumansKv1.1 Potassium ChannelKv1.2 Potassium ChannelKv1.4 Potassium ChannelMalformations of Cortical DevelopmentMiceMice, KnockoutPTEN PhosphohydrolaseSignal TransductionSirolimusTOR Serine-Threonine KinasesKv1.1 Potassium ChannelKv1.2 Potassium ChannelKv1.4 Potassium ChannelmTOR protein, mousePTEN PhosphohydrolasePten protein, mouseSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID29476105
PMCPMC5824782
OpenAlexW2803305301

What OpenQuestion holds

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Registered trials

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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.