ArticleDevelopmental cell2014
Caspase-3 cleavage of dishevelled induces elimination of postsynaptic structures.
Article in Developmental cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 44 citations in OpenAlex.
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- Caspases in the Developing Central Nervous System: Apoptosis and Beyond.Frontiers in cell and developmental biology · 2021Review
- Tumor necrosis factor alpha mediates neuromuscular synapse elimination.Cell discovery · 2020Article
- Nerve, Muscle, and Synaptogenesis.Cells · 2019Review
- Glial Contribution to Excitatory and Inhibitory Synapse Loss in Neurodegeneration.Frontiers in cellular neuroscience · 2019Review
- 13 reasons why the brain is susceptible to oxidative stress.Redox biology · 2018Review
- Errant gardeners: glial-cell-dependent synaptic pruning and neurodevelopmental disorders.Nature reviews. Neuroscience · 2017Review
- Disrupted mitochondrial genes and inflammation following stroke.Life sciences · 2016Article
- Article
- Ex vivo imaging of active caspase 3 by a FRET-based molecular probe demonstrates the cellular dynamics and localization of the protease in cerebellar granule cells and its regulation by the apoptosis-inhibiting protein survivin.Molecular neurodegeneration · 2016Article
- Pathogenesis of myasthenia gravis: update on disease types, models, and mechanisms.F1000Research · 2016Review
- The beneficial role of proteolysis in skeletal muscle growth and stress adaptation.Skeletal muscle · 2016Review
- Forced expression of muscle specific kinase slows postsynaptic acetylcholine receptor loss in a mouse model of MuSK myasthenia gravis.Physiological reports · 2015Article
- Rectification of muscle and nerve deficits in paralyzed ryanodine receptor type 1 mutant embryos.Developmental biology · 2015Article
- The Cell Death Pathway Regulates Synapse Elimination through Cleavage of Gelsolin in Caenorhabditis elegans Neurons.Cell reports · 2015Article
- Mutations in DVL1 cause an osteosclerotic form of Robinow syndrome.American journal of human genetics · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the development of vertebrate neuromuscular junction (NMJ), agrin stabilizes, whereas acetylcholine (ACh) destabilizes AChR clusters, leading to the refinement of synaptic connections. The intracellular mechanism underlying this counteractive interaction remains elusive. Here, we show that caspase-3, the effector protease involved in apoptosis, mediates elimination of AChR clusters. We found that caspase-3 was activated by cholinergic stimulation of cultured muscle cells without inducing cell apoptosis and that this activation was prevented by agrin. Interestingly, inhibition of caspase-3 attenuated ACh agonist-induced dispersion of AChR clusters. Furthermore, we identified Dishevelled1 (Dvl1), a Wnt signaling protein involved in AChR clustering, as the substrate of caspase-3. Blocking Dvl1 cleavage prevented induced dispersion of AChR clusters. Finally, inhibition or genetic ablation of caspase-3 or expression of a caspase-3-resistant form of Dvl1 caused stabilization of aneural AChR clusters. Thus, caspase-3 plays an important role in the elimination of postsynaptic structures during the development of NMJs.
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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.