ArticleThe Journal of cell biology2003
Tyrosine-phosphorylated and nonphosphorylated isoforms of alpha-dystrobrevin: roles in skeletal muscle and its neuromuscular and myotendinous junctions.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed.
- Myotendinous Junction development and repair.Journal of orthopaedic translation · 2026Review
- Five key challenges for the plasma membrane insertion of nicotinic acetylcholine receptors in cellular model systems.Molecular and cellular biochemistry · 2026Review
- Article
- Plasticity and structural alterations of mitochondria and sarcoplasmic organelles in muscles of mice deficient in α-dystrobrevin, a component of the dystrophin-glycoprotein complex.Human molecular genetics · 2024Article
- Variants in DTNA cause a mild, dominantly inherited muscular dystrophy.Acta neuropathologica · 2023Article
- 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 proteomic profile of the human myotendinous junction.iScience · 2022Article
- Tks5 Regulates Synaptic Podosome Formation and Stabilization of the Postsynaptic Machinery at the Neuromuscular Junction.International journal of molecular sciences · 2021Article
- Phosphorylation of α-dystrobrevin is essential for αkap accumulation and acetylcholine receptor stability.The Journal of biological chemistry · 2020Article
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- Arhgef5 Binds α-Dystrobrevin 1 and Regulates Neuromuscular Junction Integrity.Frontiers in molecular neuroscience · 2020Article
- Near-Random Distribution of Chromosome-Derived Circular DNA in the Condensed Genome of Pigeons and the Larger, More Repeat-Rich Human Genome.Genome biology and evolution · 2020Article
- Vezatin is required for the maturation of the neuromuscular synapse.Molecular biology of the cell · 2019Article
- Sarcoglycan Alpha Mitigates Neuromuscular Junction Decline in Aged Mice by Stabilizing LRP4.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Fundamental Molecules and Mechanisms for Forming and Maintaining Neuromuscular Synapses.International journal of molecular sciences · 2018Review
- Liprin-α-1 is a novel component of the murine neuromuscular junction and is involved in the organization of the postsynaptic machinery.Scientific reports · 2017Article
- Spatial distribution and molecular dynamics of dystrophin glycoprotein components at the neuromuscular junctionJournal of cell science · 2017Article
- Α-Dystrobrevin-1 recruits Grb2 and α-catulin to organize neurotransmitter receptors at the neuromuscular junction.Journal of cell science · 2016Article
- Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Physiological reviews · 2016Review
- The Dystrophin Complex: Structure, Function, and Implications for Therapy.Comprehensive Physiology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
alpha-Dystrobrevin (DB), a cytoplasmic component of the dystrophin-glycoprotein complex, is found throughout the sarcolemma of muscle cells. Mice lacking alphaDB exhibit muscular dystrophy, defects in maturation of neuromuscular junctions (NMJs) and, as shown here, abnormal myotendinous junctions (MTJs). In normal muscle, alternative splicing produces two main alphaDB isoforms, alphaDB1 and alphaDB2, with common NH2-terminal but distinct COOH-terminal domains. alphaDB1, whose COOH-terminal extension can be tyrosine phosphorylated, is concentrated at the NMJs and MTJs. alphaDB2, which is not tyrosine phosphorylated, is the predominant isoform in extrajunctional regions, and is also present at NMJs and MTJs. Transgenic expression of either isoform in alphaDB-/- mice prevented muscle fiber degeneration; however, only alphaDB1 completely corrected defects at the NMJs (abnormal acetylcholine receptor patterning, rapid turnover, and low density) and MTJs (shortened junctional folds). Site-directed mutagenesis revealed that the effectiveness of alphaDB1 in stabilizing the NMJ depends in part on its ability to serve as a tyrosine kinase substrate. Thus, alphaDB1 phosphorylation may be a key regulatory point for synaptic remodeling. More generally, alphaDB may play multiple roles in muscle by means of differential distribution of isoforms with distinct signaling or structural properties.
Indexed as
Identifiers
What OpenQuestion holds
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.