ArticleThe Journal of biological chemistry2014
Coordinated nuclear and synaptic shuttling of afadin promotes spine plasticity and histone modifications.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- A key role of Canoe's intrinsically disordered region in linking cell junctions to the cytoskeleton.The Journal of cell biology · 2025Article
- AF6 regulates intestinal IgA via crosstalk between intestinal epithelial cells and immune cells in inflammatory bowel disease.iScience · 2025Article
- Adaptor protein APPL1 links neuronal activity to chromatin remodeling in cultured hippocampal neurons.Journal of molecular cell biology · 2021Article
- The Histone Modifications of Neuronal Plasticity.Neural plasticity · 2021Review
- How the epigenome integrates information and reshapes the synapse.Nature reviews. Neuroscience · 2019Review
- Afadin cooperates with Claudin-2 to promote breast cancer metastasis.Genes & development · 2019Article
- Cyto-nuclear shuttling of afadin is required for rapid estradiol-mediated modifications of histone H3.Neuropharmacology · 2018Article
- Cooperation of Genomic and Rapid Nongenomic Actions of Estrogens in Synaptic Plasticity.Molecular neurobiology · 2017Review
- Control of Dendritic Spine Morphological and Functional Plasticity by Small GTPases.Neural plasticity · 2016Review
- Afadin is localized at cell-cell contact sites in mesangial cells and regulates migratory polarity.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Loss of polarity protein AF6 promotes pancreatic cancer metastasis by inducing Snail expression.Nature communications · 2015Article
- Actin-tethered junctional complexes in angiogenesis and lymphangiogenesis in association with vascular endothelial growth factor.BioMed research international · 2015Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The ability of a neuron to transduce extracellular signals into long lasting changes in neuronal morphology is central to its normal function. Increasing evidence shows that coordinated regulation of synaptic and nuclear signaling in response to NMDA receptor activation is crucial for long term memory, synaptic tagging, and epigenetic signaling. Although mechanisms have been proposed for synapse-to-nuclear communication, it is unclear how signaling is coordinated at both subcompartments. Here, we show that activation of NMDA receptors induces the bi-directional and concomitant shuttling of the scaffold protein afadin from the cytosol to the nucleus and synapses. Activity-dependent afadin nuclear translocation peaked 2 h post-stimulation, was independent of protein synthesis, and occurred concurrently with dendritic spine remodeling. Moreover, activity-dependent afadin nuclear translocation coincides with phosphorylation of histone H3 at serine 10 (H3S10p), a marker of epigenetic modification. Critically, blocking afadin nuclear accumulation attenuated activity-dependent dendritic spine remodeling and H3 phosphorylation. Collectively, these data support a novel model of neuronal nuclear signaling whereby dual-residency proteins undergo activity-dependent bi-directional shuttling from the cytosol to synapses and the nucleus, coordinately regulating dendritic spine remodeling and histone modifications.
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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.