ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
The Ets transcription factor GABP is required for postsynaptic differentiation in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 76 citations in OpenAlex.
- GABP Promotes Mesangial Cell Proliferation and Renal Fibrosis Through GLI1 in Diabetic Nephropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Activity-dependent transcriptional programs in memory regulate motor recovery after stroke.Communications biology · 2024Article
- MiR-142a-3p: A novel ACh receptor transcriptional regulator in association with peripheral nerve injury.Molecular therapy. Nucleic acids · 2022Article
- Nerve-dependent distribution of subsynaptic type 1 inositol 1,4,5-trisphosphate receptor at the neuromuscular junction.The Journal of general physiology · 2022Article
- Recent insights into neuromuscular junction biology in Duchenne muscular dystrophy: Impacts, challenges, and opportunities.EBioMedicine · 2020Review
- Adrenergic-Independent Signaling via CHRNA2 Regulates Beige Fat Activation.Developmental cell · 2020Article
- Modeling the transport of nuclear proteins along single skeletal muscle cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Ets transcription factor GABP controls T cell homeostasis and immunity.Nature communications · 2017Article
- Pre- and postsynaptic changes in the neuromuscular junction in dystrophic mice.Frontiers in physiology · 2015Article
- Targeting tetramer-forming GABPβ isoforms impairs self-renewal of hematopoietic and leukemic stem cells.Cell stem cell · 2012Article
- Molecular control of neuromuscular junction development.Journal of cachexia, sarcopenia and muscle · 2012Article
- The ETS transcription factors ELK1 and GABPA regulate different gene networks to control MCF10A breast epithelial cell migration.PloS one · 2012Article
- Targeting artificial transcription factors to the utrophin A promoter: effects on dystrophic pathology and muscle function.The Journal of biological chemistry · 2008Article
- GA-binding protein is dispensable for neuromuscular synapse formation and synapse-specific gene expression.Molecular and cellular biology · 2007Article
- Targeting of the ETS factor GABPalpha disrupts neuromuscular junction synaptic function.Molecular and cellular biology · 2007Article
- PGC-1alpha regulates the neuromuscular junction program and ameliorates Duchenne muscular dystrophy.Genes & development · 2007Article
- Postsynaptic chromatin is under neural control at the neuromuscular junction.The EMBO journal · 2007Article
- Identification of a crucial site for synoviolin expression.Molecular and cellular biology · 2005Article
- Organization of synaptic myonuclei by Syne proteins and their role during the formation of the nerve-muscle synapse.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At chemical synapses, neurotransmitter receptors are concentrated in the postsynaptic membrane. During the development of the neuromuscular junction, motor neurons induce aggregation of acetylcholine receptors (AChRs) underneath the nerve terminal by the redistribution of existing AChRs and preferential transcription of the AChR subunit genes in subsynaptic myonuclei. Neural agrin, when expressed in nonsynaptic regions of muscle fibers in vivo, activates both mechanisms resulting in the assembly of a fully functional postsynaptic apparatus. Several lines of evidence indicate that synaptic transcription of AChR genes is primarily dependent on a promoter element called N-box. The Ets-related transcription factor growth-associated binding protein (GABP) binds to this motif and has thus been suggested to regulate synaptic gene expression. Here, we assessed the role of GABP in synaptic gene expression and in the formation of postsynaptic specializations in vivo by perturbing its function during postsynaptic differentiation induced by neural agrin. We find that neural agrin-mediated activation of the AChR epsilon subunit promoter is abolished by the inhibition of GABP function. Importantly, the number of AChR aggregates formed in response to neural agrin was strongly reduced. Moreover, aggregates of acetylcholine esterase and utrophin, two additional components of the postsynaptic apparatus, were also reduced. Together, these results are the first direct in vivo evidence that GABP regulates synapse-specific gene expression at the neuromuscular junction and that GABP is required for the formation of a functional postsynaptic apparatus.
Indexed as
Identifiers
10934247PMC6772583W2129970296What Socratic 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 Socratic graph.