ArticleThe European journal of neuroscience2016
Shank-cortactin interactions control actin dynamics to maintain flexibility of neuronal spines and synapses.
Article in The European journal of neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 62 citations in OpenAlex.
- SHANK2 establishes auditory hair bundle architecture essential for mammalian hearing.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Multi-omics study reveals differential expression and phosphorylation of autophagy-related proteins in autism spectrum disorder.Scientific reports · 2025Article
- Role of Cytoskeletal Elements in Regulation of Synaptic Functions: Implications Toward Alzheimer's Disease and Phytochemicals-Based Interventions.Molecular neurobiology · 2024Review
- Differential nanoscale organization of excitatory synapses onto excitatory vs. inhibitory neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- TheFrontiers in synaptic neuroscience · 2024Article
- Identification of novelFrontiers in neuroscience · 2023Article
- Dendritic Spine in Autism Genetics: Whole-Exome Sequencing Identifying De Novo Variant ofChildren (Basel, Switzerland) · 2022Article
- Association of SHANK Family with Neuropsychiatric Disorders: An Update on Genetic and Animal Model Discoveries.Cellular and molecular neurobiology · 2022Review
- SH3- and actin-binding domains connect ADNP and SHANK3, revealing a fundamental shared mechanism underlying autism.Molecular psychiatry · 2022Article
- Integrated Analysis of Cortex Single-Cell Transcriptome and Serum Proteome Reveals the Novel Biomarkers in Alzheimer's Disease.Brain sciences · 2022Article
- Novel role of the synaptic scaffold protein Dlgap4 in ventricular surface integrity and neuronal migration during cortical development.Nature communications · 2022Article
- Cortactin in Lung Cell Function and Disease.International journal of molecular sciences · 2022Review
- Activity dependent dissociation of the Homer1 interactome.Scientific reports · 2022Article
- mTOR-Dependent Spine Dynamics in Autism.Frontiers in molecular neuroscience · 2022Review
- The Shank3Frontiers in neuroscience · 2022Article
- Actin capping protein regulates postsynaptic spine development through CPI-motif interactions.Frontiers in molecular neuroscience · 2022Article
- Cortactin Contributes to Activity-Dependent Modulation of Spine Actin Dynamics and Spatial Memory Formation.Cells · 2021Article
- Autism-associatedeLife · 2021Article
- DNA Methylation in Babies Born to Nonsmoking Mothers Exposed to Secondhand Smoke during Pregnancy: An Epigenome-Wide Association Study.Environmental health perspectives · 2021Article
- Abl2:Cortactin Interactions Regulate Dendritic Spine Stability via Control of a Stable Filamentous Actin Pool.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The family of Shank scaffolding molecules (comprising Shank1, 2 and 3) are core components of the postsynaptic density (PSD) in neuronal synapses. Shanks link surface receptors to other scaffolding molecules within the PSD, as well as to the actin cytoskeleton. However, determining the function of Shank proteins in neurons has been complicated because the different Shank isoforms share a very high degree of sequence and domain homology. Therefore, to control Shank content while minimizing potential compensatory effects, a miRNA-based knockdown strategy was developed to reduce the expression of all synaptically targeted Shank isoforms simultaneously in rat hippocampal neurons. Using this approach, a strong (>75%) reduction in total Shank protein levels was achieved at individual dendritic spines, prompting an approximately 40% decrease in mushroom spine density. Furthermore, Shank knockdown reduced spine actin levels and increased sensitivity to the actin depolymerizing agent Latrunculin A. A SHANK2 mutant lacking the proline-rich cortactin-binding motif (SHANK2-ΔPRO) was unable to rescue these defects. Furthermore, Shank knockdown reduced cortactin levels in spines and increased the mobility of spine cortactin as measured by single-molecule tracking photoactivated localization microscopy, suggesting that Shank proteins recruit and stabilize cortactin at the synapse. Furthermore, it was found that Shank knockdown significantly reduced spontaneous remodelling of synapse morphology that could not be rescued by the SHANK2-ΔPRO mutant. It was concluded that Shank proteins are key intermediates between the synapse and the spine interior that, via cortactin, permit the actin cytoskeleton to dynamically regulate synapse morphology and function.
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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.