ArticleJournal of molecular psychiatry2016
αT-catenin in restricted brain cell types and its potential connection to autism.
Article in Journal of molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Systematic Review and Bioinformatic Analysis of microRNA Expression in Autism Spectrum Disorder Identifies Pathways Associated With Cancer, Metabolism, Cell Signaling, and Cell Adhesion.Frontiers in psychiatry · 2021Pooled it
- Sexual Selection as a Driver of Shared Neural and Reproductive Mechanisms.International journal of molecular sciences · 2026Review
- Characterization of genomic regions escaping epigenetic reprogramming in sheep.Environmental epigenetics · 2024Article
- LRRTM3 Genetic Variations, rs1925575, and rs1925608 Contributed to Autism Spectrum Disorder Trait Severity: An Observation in The Indian Probands.International journal of molecular and cellular medicine · 2023Article
- Alpha-T-catenin is expressed in peripheral nerves as a constituent of Schwann cell adherens junctions.Biology open · 2022Article
- A pilot study that provides evidence of epigenetic changes among mother-child pairs living proximal to mining in the US.Environmental geochemistry and health · 2022Article
- SPATA33 affects the formation of cell adhesion complex by interacting with CTNNA3 in TM4 cells.Cell and tissue research · 2022Article
- Traumatic events during childhood and its risks to substance use in adulthood: an observational and genome-wide by environment interaction study in UK Biobank.Translational psychiatry · 2021Observational
- The depression GWAS risk allele predicts smaller cerebellar gray matter volume and reduced SIRT1 mRNA expression in Chinese population.Translational psychiatry · 2019Article
- Exome sequencing in multiple sclerosis families identifies 12 candidate genes and nominates biological pathways for the genesis of disease.PLoS genetics · 2019Article
- Commonality in dysregulated expression of gene sets in cortical brains of individuals with autism, schizophrenia, and bipolar disorder.Translational psychiatry · 2019Article
- Article
- APOE hypermethylation is associated with autism spectrum disorder in a Chinese population.Experimental and therapeutic medicine · 2018Article
- αT-catenin: A developmentally dispensable, disease-linked member of the α-catenin family.Tissue barriers · 2018Review
- Cardiomyocytes of the Heart and Pulmonary Veins: Novel Contributors to Asthma?American journal of respiratory cell and molecular biology · 2017Review
- Distinct intramolecular interactions regulate autoinhibition of vinculin binding in αT-catenin and αE-catenin.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundRecent genetic association studies have linked the cadherin-based adherens junction protein alpha-T-catenin (αT-cat, CTNNA3) with the development of autism. Where αT-cat is expressed in the brain, and how its loss could contribute to this disorder, are entirely unknown.
methodsWe used the αT-cat knockout mouse to examine the localization of αT-cat in the brain, and we used histology and immunofluorescence analysis to examine the neurobiological consequences of its loss.
resultsWe found that αT-cat comprises the ependymal cell junctions of the ventricles of the brain, and its loss led to compensatory upregulation of αE-cat expression. Notably, αT-cat was not detected within the choroid plexus, which relies on cell junction components common to typical epithelial cells. While αT-cat was not detected in neurons of the cerebral cortex, it was abundantly detected within neuronal structures of the molecular layer of the cerebellum. Although αT-cat loss led to no overt differences in cerebral or cerebellar structure, RNA-sequencing analysis from wild type versus knockout cerebella identified a number of disease-relevant signaling pathways associated with αT-cat loss, such as GABA-A receptor activation.
conclusionsThese findings raise the possibility that the genetic associations between αT-cat and autism may be due to ependymal and cerebellar defects, and highlight the potential importance of a seemingly redundant adherens junction component to a neurological disorder.
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Registered trials
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.