Evidence map›Paper›PMID 34100899›Full record

ArticleBiology open2021

Postnatal expression profiles of atypical cadherin FAT1 suggest its role in autism.

Jeannine A Frei, Cheryl Brandenburg, Jonathan E Nestor, Didier M Hodzic, Celine Plachez, Helen McNeill, Derek M Dykxhoorn, Michael W Nestor, Gene J Blatt, Yu-Chih Lin

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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 at 4 institutions in 1 country.

Jeannine A FreiProgram in Neuroscience, Hussman Institute for Autism, Baltimore, MD 21201, USA.
Cheryl BrandenburgProgram in Neuroscience, Hussman Institute for Autism, Baltimore, MD 21201, USA.
Jonathan E NestorProgram in Neuroscience, Hussman Institute for Autism, Baltimore, MD 21201, USA.
Didier M HodzicDepartment of Developmental Biology, Washington University School of Medicine, St Louis, MO 63110, USA.
Celine PlachezProgram in Neuroscience, Hussman Institute for Autism, Baltimore, MD 21201, USA.ORCID 0000-0001-5207-6208
Helen McNeillDepartment of Developmental Biology, Washington University School of Medicine, St Louis, MO 63110, USA.
Derek M DykxhoornHussman Institute for Human Genomics and John T. Macdonald Foundation Department of Human Genetics, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.
Michael W NestorProgram in Neuroscience, Hussman Institute for Autism, Baltimore, MD 21201, USA.
Gene J BlattProgram in Neuroscience, Hussman Institute for Autism, Baltimore, MD 21201, USA.
Yu-Chih LinProgram in Neuroscience, Hussman Institute for Autism, Baltimore, MD 21201, USA.
Hussman Institute for Autism · USUniversity of Maryland, Baltimore · USWashington University in St. Louis · USUniversity of Miami · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic studies have linked FAT1 (FAT atypical cadherin 1) with autism spectrum disorder (ASD); however, the role that FAT1 plays in ASD remains unknown. In mice, the function of Fat1 has been primarily implicated in embryonic nervous system development with less known about its role in postnatal development. We show for the first time that FAT1 protein is expressed in mouse postnatal brains and is enriched in the cerebellum, where it localizes to granule neurons and Golgi cells in the granule layer, as well as inhibitory neurons in the molecular layer. Furthermore, subcellular characterization revealed FAT1 localization in neurites and soma of granule neurons, as well as being present in the synaptic plasma membrane and postsynaptic densities. Interestingly, FAT1 expression was decreased in induced pluripotent stem cell (iPSC)-derived neural precursor cells (NPCs) from individuals with ASD. These findings suggest a novel role for FAT1 in postnatal development and may be particularly important for cerebellum function. As the cerebellum is one of the vulnerable brain regions in ASD, our study warrants further investigation of FAT1 in the disease etiology.

Indexed as

Disease SusceptibilityAnimalsAutistic DisorderBiomarkersCadherinsCerebellumDisease Models, AnimalGene Expression ProfilingGene Expression RegulationHippocampusInduced Pluripotent Stem CellsInterneuronsMiceNeuritesProtein TransportTranscriptomeBiomarkersCadherinsfat1 protein, mouseAutismCadherinCerebellumFAT1Granule cellsNeural precursor cells

Identifiers

PMID34100899
PMCPMC8214424
OpenAlexW3160629642

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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.