ArticleNeuron2008
A mammalian homolog of Drosophila tumorous imaginal discs, Tid1, mediates agrin signaling at the neuromuscular junction.
Article in Neuron, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 75 citations in OpenAlex.
- Muscle-Specific Kinase Signaling and Its Therapeutic Potential.Muscle & nerve · 2026Review
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Analysis of theCells · 2024Article
- A peptide derived from TID1S rescues frataxin deficiency and mitochondrial defects in FRDA cellular models.Frontiers in pharmacology · 2024Article
- Maturation of a postsynaptic domain: Role of small Rho GTPases in organising nicotinic acetylcholine receptor aggregates at the vertebrate neuromuscular junction.Journal of anatomy · 2022Review
- Putting human Tid-1 in context: an insight into its role in the cell and in different disease states.Cell communication and signaling : CCS · 2022Review
- Mitochondrial "dysmorphology" in variant classification.Human genetics · 2022Article
- Characterisation of the heat shock protein Tid and its involvement in stress response regulation inFrontiers in physiology · 2022Article
- An Inside Job: Molecular Determinants for Postsynaptic Localization of Nicotinic Acetylcholine Receptors.Molecules (Basel, Switzerland) · 2021Review
- Motor function recovery: deciphering a regenerative niche at the neuromuscular synapse.Biological reviews of the Cambridge Philosophical Society · 2021Review
- Study on the differential proteomics of rat hippocampal mitochondria during deep hypothermic circulatory arrest.Annals of translational medicine · 2021Article
- The Neuromuscular Junction in Health and Disease: Molecular Mechanisms Governing Synaptic Formation and Homeostasis.Frontiers in molecular neuroscience · 2020Review
- Myasthenia Gravis: From the Viewpoint of Pathogenicity Focusing on Acetylcholine Receptor Clustering, Trans-Synaptic Homeostasis and Synaptic Stability.Frontiers in molecular neuroscience · 2020Article
- Synaptic Homeostasis and Its Immunological Disturbance in Neuromuscular Junction Disorders.International journal of molecular sciences · 2017Review
- Mitochondrial co-chaperone protein Tid1 is required for energy homeostasis during skeletal myogenesis.Stem cell research & therapy · 2016Article
- Neuregulin1 displayed on motor axons regulates terminal Schwann cell-mediated synapse elimination at developing neuromuscular junctions.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Tid1, the Mammalian Homologue of Drosophila Tumor Suppressor Tid56, Mediates Macroautophagy by Interacting with Beclin1-containing Autophagy Protein Complex.The Journal of biological chemistry · 2015Article
- Essential role of TID1 in maintaining mitochondrial membrane potential homogeneity and mitochondrial DNA integrity.Molecular and cellular biology · 2014Article
- Wnt signaling in skeletal muscle dynamics: myogenesis, neuromuscular synapse and fibrosis.Molecular neurobiology · 2014Review
- Structural mechanisms of the agrin-LRP4-MuSK signaling pathway in neuromuscular junction differentiation.Cellular and molecular life sciences : CMLS · 2013Review
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4 authors at 2 institutions in 1 country.
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Abstract
Motoneuron-derived agrin clusters nicotinic acetylcholine receptors (AChRs) in mammalian muscle cells. We used two-hybrid screens to identify a protein, tumorous imaginal discs (Tid1), that binds to the cytoplasmic domain of muscle-specific kinase (MuSK), a major component of the agrin receptor. Like MuSK, Tid1 colocalizes with AChRs at developing, adult, and denervated motor endplates. Knockdown of Tid1 by short hairpin RNA (shRNA) in skeletal muscle fibers dispersed synaptic AChR clusters and impaired neuromuscular transmission. In cultured myotubes, Tid1 knockdown inhibited AChR clustering, as well as agrin-induced activation of the Rac and Rho small GTPases and tyrosine phosphorylation of the AChR, without affecting MuSK activation. Tid1 knockdown also decreased Dok-7-induced clustering of AChRs. Overexpression of the N-terminal half of Tid1 induced agrin- and MuSK-independent phosphorylation and clustering of AChRs. These results demonstrate that Tid1 is an essential component of the agrin signaling pathway, crucial for synaptic development.
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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.