ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
The knockdown of αkap alters the postsynaptic apparatus of neuromuscular junctions in living mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Early postsynaptic instability and acetylcholine receptor compartmentalization precede neuromuscular synapse dismantling.Communications biology · 2026Article
- Distinct roles of the dystrophin-glycoprotein complex: α-dystrobrevin and α-syntrophin in the maintenance of the postsynaptic apparatus of the neuromuscular synapse.Human molecular genetics · 2022Article
- The Metabolic Stability of the Nicotinic Acetylcholine Receptor at the Neuromuscular Junction.Cells · 2021Review
- Phosphorylation of α-dystrobrevin is essential for αkap accumulation and acetylcholine receptor stability.The Journal of biological chemistry · 2020Article
- The disassembly of the neuromuscular synapse in high-fat diet-induced obese male mice.Molecular metabolism · 2020Article
- Analysis of the CaMKIIα and β splice-variant distribution among brain regions reveals isoform-specific differences in holoenzyme formation.Scientific reports · 2018Article
- Viral delivery ofDisease models & mechanisms · 2017Article
- Spatial distribution and molecular dynamics of dystrophin glycoprotein components at the neuromuscular junctionJournal of cell science · 2017Article
- Deletion ofMolecular and cellular biology · 2017Article
- AChRs Are Essential for the Targeting of Rapsyn to the Postsynaptic Membrane of NMJs in Living Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
A muscle-specific nonkinase anchoring protein (αkap), encoded within the calcium/calmodulin kinase II (camk2) α gene, was recently found to control the stability of acetylcholine receptor (AChR) clusters on the surface of cultured myotubes. However, it remains unknown whether this protein has any effect on receptor stability and the maintenance of the structural integrity of neuromuscular synapses in vivo. By knocking down the endogenous expression of αkap in mouse sternomastoid muscles with shRNA, we found that the postsynaptic receptor density was dramatically reduced, the turnover rate of receptors at synaptic sites was significantly increased, and the insertion rates of both newly synthesized and recycled receptors into the postsynaptic membrane were depressed. Moreover, we found that αkap shRNA knockdown impaired synaptic structure as postsynaptic AChR clusters and their associated postsynaptic scaffold proteins within the neuromuscular junction were completely eliminated. These results provide new mechanistic insight into the role of αkap in regulating the stability of the postsynaptic apparatus of neuromuscular synapses.
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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.