Evidence map›Paper›PMID 33786950›Full record

ArticleBrain pathology (Zurich, Switzerland)2021

Upregulation of the pathogenic transcription factor SPI1/PU.1 in tuberous sclerosis complex and focal cortical dysplasia by oxidative stress.

Till S Zimmer, Anatoly Korotkov, Susan Zwakenberg, Floor E Jansen, Fried J T Zwartkruis, Nicholas R Rensing, Michael Wong, Angelika Mühlebner, Erwin A van Vliet, Eleonora Aronica and 1 more

Open access · goldAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

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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

11 authors at 5 institutions in 3 countries.

Till S ZimmerDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.ORCID 0000-0002-6869-3697
Anatoly KorotkovDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.ORCID 0000-0002-8313-6282
Susan ZwakenbergCenter for Molecular Medicine, Molecular Cancer Research, University Medical Center Utrecht, Utrecht, the Netherlands.
Floor E JansenDepartment of Pediatric Neurology, Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands.
Fried J T ZwartkruisCenter for Molecular Medicine, Molecular Cancer Research, University Medical Center Utrecht, Utrecht, the Netherlands.
Nicholas R RensingDepartment of Neurology, Washington University, Saint Louis, MO, USA.
Michael WongDepartment of Neurology, Washington University, Saint Louis, MO, USA.
Angelika MühlebnerDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.ORCID 0000-0001-9102-7353
Erwin A van VlietDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.ORCID 0000-0001-5747-3202
Eleonora AronicaDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
James D MillsDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
University Medical Center Utrecht · NLAmsterdam Neuroscience · NLWashington University in St. Louis · USEpilepsy Research UK · GBNetherlands Institute for Neuroscience · NL

Funding

MECHANISMS OF BRAIN DYSFUNCTION IN TUBEROUS SCLEROSISR01NS056872 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2006 to 2019
$4.0M
NINDS NIH HHS R01 NS056872
6 · The paper itself

Abstract

Tuberous sclerosis complex (TSC) is a congenital disorder characterized by cortical malformations and concomitant epilepsy caused by loss-of-function mutations in the mTOR suppressors TSC1 or TSC2. While the underlying molecular changes caused by mTOR activation in TSC have previously been investigated, the drivers of these transcriptional change have not been fully elucidated. A better understanding of the perturbed transcriptional regulation could lead to the identification of novel pathways for therapeutic intervention not only in TSC, but other genetic epilepsies in which mTOR activation plays a key role, such as focal cortical dysplasia 2b (FCD). Here, we analyzed RNA sequencing data from cortical tubers and a tsc2

Indexed as

AnimalsAstrocytesBrainHumansMalformations of Cortical DevelopmentMice, TransgenicNeuronsOxidative StressProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTuberous SclerosisTuberous Sclerosis Complex 2 ProteinUp-RegulationProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTSC2 protein, humanTsc2 protein, mouseTuberous Sclerosis Complex 2 Proteinbrain inflammationepilepsyfocal cortical dysplasiamTORoxidative stresstuberous sclerosis complex

Identifiers

PMID33786950
PMCPMC8412124
OpenAlexW3144639711

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.