Evidence map›Paper›PMID 32294447›Full record

ArticleCell reports2020

Enhancing WNT Signaling Restores Cortical Neuronal Spine Maturation and Synaptogenesis in Tbr1 Mutants.

Siavash Fazel Darbandi, Sarah E Robinson Schwartz, Emily Ling-Lin Pai, Amanda Everitt, Marc L Turner, Benjamin N R Cheyette, A Jeremy Willsey, Matthew W State, Vikaas S Sohal, John L R Rubenstein

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Serum Levels of Wnt/β-catenin Pathway Regulators Dkk-1, PORCN, Notum, and Tiki-1 in Children with Autism Spectrum Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
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  3. Article
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  6. Detailed phenotyping of Tbr1-2A-CreER knock-in mice demonstrates significant impacts on TBR1 protein levels and axon development.Autism research : official journal of the International Society for Autism Research · 2025
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  12. Review
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  16. Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023
    Article
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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

10 authors at 2 institutions in 1 country.

Siavash Fazel DarbandiDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
Sarah E Robinson SchwartzDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
Emily Ling-Lin PaiDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
Amanda EverittInstitute for Neurodegenerative Diseases, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
Marc L TurnerDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
Benjamin N R CheyetteDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
A Jeremy WillseyDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Institute for Neurodegenerative Diseases, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Quantitative Biosciences Institute (QBI), University of California, San Francisco, San Francisco, CA 94143, USA.
Matthew W StateDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Quantitative Biosciences Institute (QBI), University of California, San Francisco, San Francisco, CA 94143, USA.
Vikaas S SohalDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Kavli Institute for Fundamental Neuroscience and Sloan-Swartz Center for Theoretical Neurobiology, University of California, San Francisco, San Francisco, CA 94143, USA.
John L R RubensteinDepartment of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: john.rubenstein@ucsf.edu.
University of California, San Francisco · USQuantitative BioSciences · US

Funding

Genetic Studies of Cortex Structure and DevelopmentR01NS099099 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2016 to 2025
$6.4M
GENETIC STUDIES OF CORTEX STRUCTURE AND DEVELOPMENTR01NS034661 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 1996 to 2015
$4.6M
Cellular and synaptic mechanisms for dopaminergic modulation of prefrontal cortexR01MH100292 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SOHAL, VIKAAS SINGH · 2013 to 2017
$2.5M
Restoring cognition by optogenetically rescuing gamma rhythms in PFC interneuronsR01MH106507 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SOHAL, VIKAAS SINGH · 2015 to 2019
$2.0M
NIMH NIH HHS R01 MH100292NIMH NIH HHS R01 MH106507NINDS NIH HHS R01 NS034661NINDS NIH HHS R01 NS099099
6 · The paper itself

Abstract

Tbr1 is a high-confidence autism spectrum disorder (ASD) gene encoding a transcription factor with distinct pre- and postnatal functions. Postnatally, Tbr1 conditional knockout (CKO) mutants and constitutive heterozygotes have immature dendritic spines and reduced synaptic density. Tbr1 regulates expression of several genes that underlie synaptic defects, including a kinesin (Kif1a) and a WNT-signaling ligand (Wnt7b). Furthermore, Tbr1 mutant corticothalamic neurons have reduced thalamic axonal arborization. LiCl and a GSK3β inhibitor, two WNT-signaling agonists, robustly rescue the dendritic spines and the synaptic and axonal defects, suggesting that this could have relevance for therapeutic approaches in some forms of ASD.

Indexed as

AnimalsAutism Spectrum DisorderDendritic SpinesDNA-Binding ProteinsFemaleHEK293 CellsHumansMaleMiceMice, Inbred C57BLMice, TransgenicNeurogenesisNeuronsSynapsesT-Box Domain ProteinsThalamusDNA-Binding ProteinsT-Box Domain ProteinsTbr1 protein, mouseASDcortexexcitatory neuronLiCl treatmentsocial deficitspine maturationsynaptogenesisTbr1WNT-signaling

Identifiers

PMID32294447
PMCPMC7473600
OpenAlexW3015875450

What OpenQuestion 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 OpenQuestion graph.