ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Neuronal nicotinic synapse assembly requires the adenomatous polyposis coli tumor suppressor protein.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 66 citations in OpenAlex.
- APC in the nervous system.Medical molecular morphology · 2026Review
- End-binding protein 1 regulates the metabolic fate of CD4Frontiers in immunology · 2023Article
- A Deficiency of the Psychiatric Risk Gene DLG2/PSD-93 Causes Excitatory Synaptic Deficits in the Dorsolateral Striatum.Frontiers in molecular neuroscience · 2022Article
- Epigenomic Changes after Acupuncture Treatment in Patients Suffering from Burnout.Complementary medicine research · 2022Observational
- Decreased Podocyte Vesicle Transcytosis and Albuminuria inInternational journal of molecular sciences · 2021Article
- An Inside Job: Molecular Determinants for Postsynaptic Localization of Nicotinic Acetylcholine Receptors.Molecules (Basel, Switzerland) · 2021Review
- Expression and Manipulation of the APC-β-Catenin Pathway During Peripheral Neuron Regeneration.Scientific reports · 2018Article
- Social Stimulus Causes Aberrant Activation of the Medial Prefrontal Cortex in a Mouse Model With Autism-Like Behaviors.Frontiers in synaptic neuroscience · 2018Article
- Regulatory single nucleotide polymorphisms (rSNPs) at the promoters 1A and 1B of the human APC gene.BMC genetics · 2016Article
- A conceptual view at microtubule plus end dynamics in neuronal axons.Brain research bulletin · 2016Review
- 6-OHDA-Induced Changes in Parkinson's Disease-Related Gene Expression are not Affected by the Overexpression of PGAM5 in In Vitro Differentiated Embryonic Mesencephalic Cells.Cellular and molecular neurobiology · 2015Article
- 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
- Microtubule plus-end tracking protein CLASP2 regulates neuronal polarity and synaptic function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Wnt signaling in neuromuscular junction development.Cold Spring Harbor perspectives in biology · 2012Review
- Colocalization of APC and PSD-95 in the nerve fiber as well as in the post-synapse of matured neurons.Medical molecular morphology · 2012Article
- PMCA2 via PSD-95 controls calcium signaling by α7-containing nicotinic acetylcholine receptors on aspiny interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Article
- Adenomatous polyposis coli is essential for both neuronal differentiation and maintenance of adult neural stem cells in subventricular zone and hippocampus.Stem cells (Dayton, Ohio) · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Normal cognitive and autonomic functions require nicotinic synaptic signaling. Despite the physiological importance of these synapses, little is known about molecular mechanisms that direct their assembly during development. We show here that the tumor-suppressor protein adenomatous polyposis coli (APC) functions in localizing alpha3-nicotinic acetylcholine receptors (nAChRs) to neuronal postsynaptic sites. Our quantitative confocal microscopy studies indicate that APC is selectively enriched at cholinergic synapses; APC surface clusters are juxtaposed to synaptic vesicle clusters and colocalize with alpha3-nAChRs but not with the neighboring synaptic glycine receptors or perisynaptic alpha7-nAChRs on chick ciliary ganglion (CG) neurons. We identify PSD (postsynaptic density)-93, beta-catenin, and microtubule end binding protein EB1 as APC binding partners. PSD-93 and beta-catenin are also enriched at alpha3-nAChR postsynaptic sites. EB1 shows close proximity to and partial overlap with alpha3-nAChR and APC surface clusters. We tested the role of APC in neuronal nicotinic synapse assembly by using retroviral-mediated in vivo overexpression of an APC dominant-negative (APC-dn) peptide to block the interaction of endogenous APC with both EB1 and PSD-93 during synapse formation in CG neurons. The overexpressed APC-dn led to dramatic decreases in alpha3-nAChR surface levels and clusters. Effects were specific to alpha3-nAChR postsynaptic sites; synaptic glycine receptor and perisynaptic alpha7-nAChR clusters were not altered. In addition, APC-dn also reduced surface membrane-associated clusters of PSD-93 and EB1. The results show that APC plays a key role in organizing excitatory cholinergic postsynaptic specializations in CG neurons. We identify APC as the first nonreceptor protein to function in localizing nAChRs to neuronal synapses in vivo.
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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.