ArticleCommunicative & integrative biology2008
The role of Wnt/beta-catenin signaling in postsynaptic differentiation.
Article in Communicative & integrative biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- FUS-ALS hiPSC-derived astrocytes impair human motor units through both gain-of-toxicity and loss-of-support mechanisms.Molecular neurodegeneration · 2023Article
- Intercellular protein-protein interactions at synapses.Protein & cell · 2014Review
- Wnt signaling in skeletal muscle dynamics: myogenesis, neuromuscular synapse and fibrosis.Molecular neurobiology · 2014Review
- Frizzled-9 impairs acetylcholine receptor clustering in skeletal muscle cells.Frontiers in cellular neuroscience · 2014Article
- Identification of candidate genes encoding an LDL-C QTL in baboons.Journal of lipid research · 2013Article
- WNTs tune up the neuromuscular junction.Nature reviews. Neuroscience · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synapses are basic units that mediate the communication between neurons and their target cells. The formation of synapse is regulated by secreted factors, receptors, adhesion molecules and intracellular signaling molecules. The interplay between positive and negative factors determines synapse assembling, remodeling and elimination, resulting in the formation of precise synaptic connections. However, compared to the abundant identified positive factors, negative factors are largely unknown. We have recently shown that Wnt3a acts as a negative factor that inhibits postsynaptic differentiation at the neuromuscular junction (NMJ), the synapse formed between motor neurons and skeletal muscle fibers. The clustering of acetylcholine receptor (AChR) guarantees efficient and accurate neurotransmission and is a hallmark for postsynaptic differentiation at the NMJ. We found that treatment with Wnt3a or upregulation of beta-catenin inhibited the formation of AChR clusters. Furthermore, we investigated the underlying mechanism and found that Wnt/beta-catenin signaling negatively regulated AChR clustering by downregulating the expression of Rapsyn, an AChR-associated protein required for formation and stabilization of AChR clusters.
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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.