ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Differential regulation of transmitter release by alternatively spliced forms of synaptotagmin I.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Molecular and Functional Characterization of Bacopa monniera: A Retrospective Review.Evidence-based complementary and alternative medicine : eCAM · 2015Review
- A manual collection of Syt, Esyt, Rph3a, Rph3al, Doc2, and Dblc2 genes from 46 metazoan genomes--an open access resource for neuroscience and evolutionary biology.BMC genomics · 2010Article
- Molecular determinants and evolutionary dynamics of wobble splicing.Molecular biology and evolution · 2009Article
- Article
- Protein kinase C regulates local synthesis and secretion of a neuropeptide required for activity-dependent long-term synaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Differential expression and function of synaptotagmin 1 isoforms in Caenorhabditis elegans.Molecular and cellular neurosciences · 2007Article
- Synaptotagmin gene content of the sequenced genomes.BMC genomics · 2004Article
- Comparative analysis of tandem C2 domains from the mammalian synaptotagmin family.The Biochemical journal · 2004Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We discovered a novel alternatively spliced form of synaptotagmin I (Syt I). This splicing event is conserved over evolution and, in Aplysia, results in a two amino acid insert in the juxtamembrane domain of Syt I (Syt IVQ). Both Syt I and Syt IVQ are localized to synaptic vesicles; however, we also observed punctae that contained one or the other spliced products. Both Syt I and Syt IVQ are phosphorylated at the adjacent PKC site. Overexpression of Syt IVQ, but not of Syt I, in Aplysia neurons blocked the ability of serotonin to reverse synaptic depression. This effect is upstream of PKC activation, because neither Syt IVQ nor Syt I blocked the effects of phorbol esters on reversing synaptic depression or the effects of serotonin on facilitating nondepressed synapses. Our results demonstrate a physiological role for splicing in the juxtamembrane domain of Syt I.
Indexed as
Identifiers
12867508PMC6740547W1941552958What 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.