ArticleProceedings of the National Academy of Sciences of the United States of America2000
Molecular determinants of the functional interaction between syntaxin and N-type Ca2+ channel gating.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 104 citations in OpenAlex.
- Tissue- and cell-specific expression of a splice variant in the II-III cytoplasmic loop of Cacna1b.FEBS open bio · 2019Article
- AAV-encoded CaGene therapy · 2019Article
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- Cross talk between β subunits, intracellular CaPhysiological reports · 2018Article
- Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters.Molecular biology of the cell · 2016Article
- Surface dynamics of voltage-gated ion channels.Channels (Austin, Tex.) · 2016Review
- The Arabidopsis R-SNARE VAMP721 Interacts with KAT1 and KC1 K+ Channels to Moderate K+ Current at the Plasma Membrane.The Plant cell · 2015Article
- Cooperative endocytosis of the endosomal SNARE protein syntaxin-8 and the potassium channel TASK-1.Molecular biology of the cell · 2014Article
- Intra-membrane signaling between the voltage-gated Ca2+-channel and cysteine residues of syntaxin 1A coordinates synchronous release.Scientific reports · 2013Article
- GPCR mediated regulation of synaptic transmission.Progress in neurobiology · 2012Review
- A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis.The Journal of biological chemistry · 2012Article
- A novel motif essential for SNARE interaction with the K(+) channel KC1 and channel gating in Arabidopsis.The Plant cell · 2010Article
- A mutation in the first intracellular loop of CACNA1A prevents P/Q channel modulation by SNARE proteins and lowers exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Action potential modulates Ca2+-dependent and Ca2+-independent secretion in a sensory neuron.Biophysical journal · 2009Article
- 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
- Interaction of syntaxin with a single Kv1.1 channel: a possible mechanism for modulating neuronal excitability.Pflugers Archiv : European journal of physiology · 2007Article
- Bidirectional modulation of transmitter release by calcium channel/syntaxin interactions in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Distinct domain-dependent effect of syntaxin1A on amiloride-sensitive sodium channel (ENaC) currents in HT-29 colonic epithelial cells.International journal of biological sciences · 2006Article
- Structural transitions in the synaptic SNARE complex during Ca2+-triggered exocytosis.The Journal of cell biology · 2006Article
- Molecular identification and reconstitution of depolarization-induced exocytosis monitored by membrane capacitance.Biophysical journal · 2005Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Syntaxin is a key presynaptic protein that binds to N- and P/Q-type Ca(2+) channels in biochemical studies and affects gating of these Ca(2+) channels in expression systems and in synaptosomes. The present study was aimed at understanding the molecular basis of syntaxin modulation of N-type channel gating. Mutagenesis of either syntaxin 1A or the pore-forming alpha(1B) subunit of N-type Ca(2+) channels was combined with functional assays of N-type channel gating in a Xenopus oocyte coexpression system and in biochemical binding experiments in vitro. Our analysis showed that the transmembrane region of syntaxin and a short region within the H3 helical cytoplasmic domain of syntaxin, containing residues Ala-240 and Val-244, appeared critical for the channel modulation but not for biochemical association with the "synprint site" in the II/III loop of alpha(1B). These results suggest that syntaxin and the alpha(1B) subunit engage in two kinds of interactions: an anchoring interaction via the II/III loop synprint site and a modulatory interaction via another site located elsewhere in the channel sequence. The segment of syntaxin H3 found to be involved in the modulatory interaction would lie hidden within the four-helix structure of the SNARE complex, supporting the hypothesis that syntaxin's ability to regulate N-type Ca(2+) channels would be enabled after SNARE complex disassembly after synaptic vesicle exocytosis.
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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.