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http://purl.uniprot.org/citations/12896973http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12896973http://www.w3.org/2000/01/rdf-schema#comment"Voltage-gated calcium channels couple changes in membrane potential to neuronal functions regulated by calcium, including neurotransmitter release. Here we report that presynaptic N-type calcium channels not only control neurotransmitter release but also regulate synaptic growth at Drosophila neuromuscular junctions. In a screen for behavioral mutants that disrupt synaptic transmission, an allele of the N-type calcium channel locus (Dmca1A) was identified that caused synaptic undergrowth. The underlying molecular defect was identified as a neutralization of a charged residue in the third S4 voltage sensor. RNA interference reduction of N-type calcium channel expression also reduced synaptic growth. Hypomorphic mutations in syntaxin-1A or n-synaptobrevin, which also disrupt neurotransmitter release, did not affect synapse proliferation at the neuromuscular junction, suggesting calcium entry through presynaptic N-type calcium channels, not neurotransmitter release per se, is important for synaptic growth. The reduced synapse proliferation in Dmca1A mutants is not due to increased synapse retraction but instead reflects a role for calcium influx in synaptic growth mechanisms. These results suggest N-type channels participate in synaptic growth through signaling pathways that are distinct from those that mediate neurotransmitter release. Linking presynaptic voltage-gated calcium entry to downstream calcium-sensitive synaptic growth regulators provides an efficient activity-dependent mechanism for modifying synaptic strength."xsd:string
http://purl.uniprot.org/citations/12896973http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m306417200"xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/author"Guan Z."xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/author"Rieckhof G.E."xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/author"Yoshihara M."xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/author"Littleton J.T."xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/date"2003"xsd:gYear
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/name"J Biol Chem"xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/pages"41099-41108"xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/title"Presynaptic N-type calcium channels regulate synaptic growth."xsd:string
http://purl.uniprot.org/citations/12896973http://purl.uniprot.org/core/volume"278"xsd:string
http://purl.uniprot.org/citations/12896973http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/12896973
http://purl.uniprot.org/citations/12896973http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/12896973
http://purl.uniprot.org/uniprot/P91645#attribution-555A77E3629860BD54D7F38CC36E90B4http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/12896973
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http://purl.uniprot.org/uniprot/#_A0A4D6K2Y3-mappedCitation-12896973http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12896973
http://purl.uniprot.org/uniprot/#_B7Z0Z2-mappedCitation-12896973http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12896973
http://purl.uniprot.org/uniprot/#_M9MSE6-mappedCitation-12896973http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12896973
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http://purl.uniprot.org/uniprot/#_M9MSF1-mappedCitation-12896973http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12896973