ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
The postsynaptic adenomatous polyposis coli (APC) multiprotein complex is required for localizing neuroligin and neurexin to neuronal nicotinic synapses in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. 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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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- APC in the nervous system.Medical molecular morphology · 2026Review
- Critical Role of Rho Guanine Nucleotide Exchange Factor 4 in Brain Function.Molecular neurobiology · 2025Article
- The neuronal protein Neuroligin 1 promotes colorectal cancer progression by modulating the APC/β-catenin pathway.Journal of experimental & clinical cancer research : CR · 2022Article
- Epigenomic Changes after Acupuncture Treatment in Patients Suffering from Burnout.Complementary medicine research · 2022Observational
- 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
- Ubiquitous neurocognitive dysfunction in familial adenomatous polyposis: proof-of-concept of the role of APC protein in neurocognitive function.Hereditary cancer in clinical practice · 2020Article
- Learning impairments and molecular changes in the brain caused by β-catenin loss.Human molecular genetics · 2019Article
- Social Stimulus Causes Aberrant Activation of the Medial Prefrontal Cortex in a Mouse Model With Autism-Like Behaviors.Frontiers in synaptic neuroscience · 2018Article
- Time, space, and disorder in the expanding proteome universe.Proteomics · 2017Article
- APC conditional knock-out mouse is a model of infantile spasms with elevated neuronal β-catenin levels, neonatal spasms, and chronic seizures.Neurobiology of disease · 2017Article
- Microtubule plus-end tracking proteins in neuronal development.Cellular and molecular life sciences : CMLS · 2016Review
- Adenomatous Polyposis Coli Protein Deletion in Efferent Olivocochlear Neurons Perturbs Afferent Synaptic Maturation and Reduces the Dynamic Range of Hearing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Adenomatous polyposis coli protein deletion leads to cognitive and autism-like disabilities.Molecular psychiatry · 2014Article
- Neuroligin 2 is expressed in synapses established by cholinergic cells in the mouse brain.PloS one · 2013Article
- Article
- Wnt signaling: role in Alzheimer disease and schizophrenia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Review
- MAGUKs, synaptic development, and synaptic plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2011Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Synaptic efficacy requires that presynaptic and postsynaptic specializations align precisely and mature coordinately. The underlying mechanisms are poorly understood, however. We propose that adenomatous polyposis coli protein (APC) is a key coordinator of presynaptic and postsynaptic maturation. APC organizes a multiprotein complex that directs nicotinic acetylcholine receptor (nAChR) localization at postsynaptic sites in avian ciliary ganglion neurons in vivo. We hypothesize that the APC complex also provides retrograde signals that direct presynaptic active zones to develop in register with postsynaptic nAChR clusters. In our model, the APC complex provides retrograde signals via postsynaptic neuroligin that interacts extracellularly with presynaptic neurexin. S-SCAM (synaptic cell adhesion molecule) and PSD-93 (postsynaptic density-93) are scaffold proteins that bind to neuroligin. We identify S-SCAM as a novel component of neuronal nicotinic synapses. We show that S-SCAM, PSD-93, neuroligin and neurexin are enriched at alpha3*-nAChR synapses. PSD-93 and S-SCAM bind to APC and its binding partner beta-catenin, respectively. Blockade of selected APC and beta-catenin interactions, in vivo, leads to decreased postsynaptic accumulation of S-SCAM, but not PSD-93. Importantly, neuroligin synaptic clusters are also decreased. On the presynaptic side, there are decreases in neurexin and active zone proteins. Further, presynaptic terminals are less mature structurally and functionally. We define a novel neural role for APC by showing that the postsynaptic APC multiprotein complex is required for anchoring neuroligin and neurexin at neuronal synapses in vivo. APC human gene mutations correlate with autism spectrum disorders, providing strong support for the importance of the association, demonstrated here, between APC, neuroligin and neurexin.
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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.