ArticleHuman molecular genetics2019
Learning impairments and molecular changes in the brain caused by β-catenin loss.
Article in Human molecular genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- β-catenin deficiency in forebrain excitatory neurons induces fear memory deficits and physiological alterations.Brain communications · 2026Article
- Phase separation instead of binding strength determines target specificities of MAGUKs.Nature chemical biology · 2026Article
- Repetitive unidirectional spinal tactile stimulation engages microglial Bmal1 pathways to promote synaptic remodeling in the mPFC of adolescent VPA-exposed mice.Journal of neuroinflammation · 2025Article
- UBE3A stabilization of β-catenin preserves synaptic proteins essential for motor and cognitive functions in Angelman Syndrome.Molecular autism · 2025Article
- CTNNB1 syndrome mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- β-catenin-α-catenin and actomyosin signaling differentially regulate growth cone contours and axon undulation and branching of retinal ganglion cellsFrontiers in cellular neuroscience · 2025Article
- Inhibition of GSK3α,β rescues cognitive phenotypes in a preclinical mouse model of CTNNB1 syndrome.EMBO molecular medicine · 2024Article
- Alopecia areata-like pattern of baldness: the most recent update and the expansion of novel phenotype and genotype in the CTNNB1 gene.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Cortical Parvalbumin-Positive Interneuron Development and Function Are Altered in the APC Conditional Knockout Mouse Model of Infantile and Epileptic Spasms Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- CTNNB1 in neurodevelopmental disorders.Frontiers in psychiatry · 2023Review
- Genetic and clinical characteristics of 24 mainland Chinese patients with CTNNB1 loss-of-function variants.Molecular genetics & genomic medicine · 2022Article
- Identification of a novel de novo mutation in the CTNNB1 gene in an Iranian patient with intellectual disability.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- The extended clinical and genetic spectrum ofFrontiers in pediatrics · 2022Article
- The Spine Lab: A Short-Duration, Fully-Remote Course-Based Undergraduate Research Experience.Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience · 2021Article
- Case Report: AFrontiers in pediatrics · 2020Article
- Excessive β-Catenin in Excitatory Neurons Results in Reduced Social and Increased Repetitive Behaviors and Altered Expression of Multiple Genes Linked to Human Autism.Frontiers in synaptic neuroscience · 2020Article
- Paving the way toward treatment solutions for CTNNB1 syndrome: a patient organization perspective.Therapeutic advances in rare diseaseReview
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Intellectual disability (ID), defined as IQ<70, occurs in 2.5% of individuals. Elucidating the underlying molecular mechanisms is essential for developing therapeutic strategies. Several of the identified genes that link to ID in humans are predicted to cause malfunction of β-catenin pathways, including mutations in CTNNB1 (β-catenin) itself. To identify pathological changes caused by β-catenin loss in the brain, we have generated a new β-catenin conditional knockout mouse (β-cat cKO) with targeted depletion of β-catenin in forebrain neurons during the period of major synaptogenesis, a critical window for brain development and function. Compared with control littermates, β-cat cKO mice display severe cognitive impairments. We tested for changes in two β-catenin pathways essential for normal brain function, cadherin-based synaptic adhesion complexes and canonical Wnt (Wingless-related integration site) signal transduction. Relative to control littermates, β-cat cKOs exhibit reduced levels of key synaptic adhesion and scaffold binding partners of β-catenin, including N-cadherin, α-N-catenin, p120ctn and S-SCAM/Magi2. Unexpectedly, the expression levels of several canonical Wnt target genes were not altered in β-cat cKOs. This lack of change led us to find that β-catenin loss leads to upregulation of γ-catenin (plakoglobin), a partial functional homolog, whose neural-specific role is poorly defined. We show that γ-catenin interacts with several β-catenin binding partners in neurons but is not able to fully substitute for β-catenin loss, likely due to differences in the N-and C-termini between the catenins. Our findings identify severe learning impairments, upregulation of γ-catenin and reductions in synaptic adhesion and scaffold proteins as major consequences of β-catenin loss.
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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.