ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Syntaxin 1A supports voltage-dependent inhibition of alpha1B Ca2+ channels by Gbetagamma in chick sensory neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed.
- AGS3-based optogenetic GDI induces GPCR-independent Gβγ signalling and macrophage migration.Open biology · 2025Article
- Article
- AGS3-based optogenetic GDI induces GPCR-independent Gβγ signaling and macrophage migration.bioRxiv : the preprint server for biology · 2024Article
- New Insights Into Interactions of Presynaptic Calcium Channel Subtypes and SNARE Proteins in Neurotransmitter Release.Frontiers in molecular neuroscience · 2018Article
- Dopamine-mediated calcium channel regulation in synaptic suppression in L. stagnalis interneurons.Channels (Austin, Tex.) · 2018Article
- Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters.Molecular biology of the cell · 2016Article
- Distinct roles for Cav2.1-2.3 in activity-dependent synaptic dynamics.Journal of neurophysiology · 2014Article
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- Syntaxin 1B suppresses macropinocytosis and semaphorin 3A-induced growth cone collapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Rim1 modulates direct G-protein regulation of Ca(v)2.2 channels.Pflugers Archiv : European journal of physiology · 2011Article
- Selective disruption of the mammalian secretory apparatus enhances or eliminates calcium current modulation in nerve endings.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Modulation of calcium currents is eliminated after cleavage of a strategic component of the mammalian secretory apparatus.The Journal of physiology · 2005Article
- G-protein signaling: back to the future.Cellular and molecular life sciences : CMLS · 2005Review
- A protein phosphatase 2calpha-Ca2+ channel complex for dephosphorylation of neuronal Ca2+ channels phosphorylated by protein kinase C.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Syntaxin 1A regulation of weakly inactivating N-type Ca2+ channels.The Journal of physiology · 2004Article
- Regulation of syntaxin1A-munc18 complex for SNARE pairing in HEK293 cells.The Journal of physiology · 2004Article
- A syntaxin 1, Galpha(o), and N-type calcium channel complex at a presynaptic nerve terminal: analysis by quantitative immunocolocalization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- The impact of splice isoforms on voltage-gated calcium channel alpha1 subunits.The Journal of physiology · 2004Review
- Neurotransmitter modulation of neuronal calcium channels.Journal of bioenergetics and biomembranes · 2003Review
- Functional diversity in neuronal voltage-gated calcium channels by alternative splicing of Ca(v)alpha1.Molecular neurobiology · 2002Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
N-type Ca(2+) channels are modulated by a variety of G-protein-coupled pathways. Some pathways produce a transient, voltage-dependent (VD) inhibition of N channel function and involve direct binding of G-protein subunits; others require the activation of intermediate enzymes and produce a longer-lasting, voltage-independent (VI) form of inhibition. The ratio of VD:VI inhibition differs significantly among cell types, suggesting that the two forms of inhibition play unique physiological roles in the nervous system. In this study, we explored mechanisms capable of altering the balance of VD and VI inhibition in chick dorsal root ganglion neurons. We report that (1) VD:VI inhibition is critically dependent on the Gbetagamma concentration, with VI inhibition dominant at low Gbetagamma concentrations, and (2) syntaxin-1A (but not syntaxin-1B) shifts the ratio in favor of VD inhibition by potentiating the VD effects of Gbetagamma. Variations in expression levels of G-proteins and/or syntaxin provide the means to alter over a wide range both the extent and the rate of Ca(2+) influx through N channels.
Indexed as
Identifiers
11312278PMC6762579What 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.