ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016
Shank Modulates Postsynaptic Wnt Signaling to Regulate Synaptic Development.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Neurophysiological Profiles in a Family with Multiple SHANK3-Related Phelan-McDermid Syndrome Cases.International journal of molecular sciences · 2026Article
- Gene-specific DNA methylation responses to PbEnvironmental epigenetics · 2026Article
- A Frank Assessment of SHANK: Impacts of Pathogenic Variations in SHANK3 on Preclinical Models of Phelan McDermid Syndrome.Autism research : official journal of the International Society for Autism Research · 2025Review
- Molecular organization of central cholinergic synapses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- An N-terminal and ankyrin repeat domain interactome of Shank3 identifies the protein complex with the splicing regulator Nono in mice.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- Dual-specificity protein phosphatase 6 (DUSP6) overexpression reduces amyloid load and improves memory deficits in male 5xFAD mice.Frontiers in aging neuroscience · 2024Article
- Transmembrane protein 184B (TMEM184B) promotes expression of synaptic gene networks in the mouse hippocampus.BMC genomics · 2023Article
- Gastrointestinal Dysfunction in Genetically Defined Neurodevelopmental Disorders.Seminars in neurology · 2023Review
- Prospective One-Year Follow-Up of Sensory Processing in Phelan-McDermid Syndrome.Children (Basel, Switzerland) · 2023Article
- Drugs prescribed for Phelan-McDermid syndrome differentially impact sensory behaviors inF1000Research · 2023Article
- A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder.Experimental brain research · 2022Review
- Neuronal signalling of zinc: from detection and modulation to function.Open biology · 2022Review
- γ-secretase promotes Drosophila postsynaptic development through the cleavage of a Wnt receptor.Developmental cell · 2022Article
- Intellectual disability-associated disruption of O-GlcNAc cycling impairs habituation learning in Drosophila.PLoS genetics · 2022Article
- Synaptic dysfunction connects autism spectrum disorder and sleep disturbances: A perspective from studies in model organisms.Sleep medicine reviews · 2022Review
- Shank promotes action potential repolarization by recruiting BK channels to calcium microdomains.eLife · 2022Article
- Restoring Shank3 in the rostral brainstem of shank3ab-/- zebrafish autism models rescues sensory deficits.Communications biology · 2021Article
- Genomics Reveals the Origins of Historical Specimens.Molecular biology and evolution · 2021Article
- ALS2 regulates endosomal trafficking, postsynaptic development, and neuronal survival.The Journal of cell biology · 2021Article
- Extracellular heparan sulfate proteoglycans and glycan-binding lectins orchestrateJournal of cell science · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledProsap/Shank scaffolding proteins regulate the formation, organization, and plasticity of excitatory synapses. Mutations in SHANK family genes are implicated in autism spectrum disorder and other neuropsychiatric conditions. However, the molecular mechanisms underlying Shank function are not fully understood, and no study to date has examined the consequences of complete loss of all Shank proteins in vivo Here we characterize the single Drosophila Prosap/Shank family homolog. Shank is enriched at the postsynaptic membrane of glutamatergic neuromuscular junctions and controls multiple parameters of synapse biology in a dose-dependent manner. Both loss and overexpression of Shank result in defects in synaptic bouton number and maturation. We find that Shank regulates a noncanonical Wnt signaling pathway in the postsynaptic cell by modulating the internalization of the Wnt receptor Fz2. This study identifies Shank as a key component of synaptic Wnt signaling, defining a novel mechanism for how Shank contributes to synapse maturation during neuronal development. SIGNIFICANCE STATEMENT: Haploinsufficiency for SHANK3 is one of the most prevalent monogenic causes of autism spectrum disorder, making it imperative to understand how the Shank family regulates neurodevelopment and synapse function. We created the first animal model lacking all Shank proteins and used the Drosophila neuromuscular junction, a model glutamatergic synapse, to characterize the role of Shank at synapses. We identified a novel function of Shank in synapse maturation via regulation of Wnt signaling in the postsynaptic cell.
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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.