Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
16
datasets available to search
ShareScore release 0.9.0
Dataset results
16 results for “synaptotagmin”
Dataset for the Synaptotagmin-1 antibody screening study
<p><strong>This antibody characterization dataset is related to the F1000 research article openly available at F1000Research.</strong></p> <p><em>The dataset presented contains the following underlying raw data for study which evaluated twelve commercial antibodies against Synaptotagmin-1 in western blot, immunoprecipitation, immunofluorescence and flow cytometry. The original study is also accessible on the YCharOS Zenodo community (<a href="https://doi.org/10.5281/zenodo.12666747">https://doi.org/10.5281/zenodo.12666747</a>).</em></p> <p><em>The Dataset is in the format of a zip file. Once downloaded, please expand the zip file to access the folders containing the underlying data for Western blot (Wb), immunoprecipitation (IP) and immunofluorescence (IF).</em></p>
All-atom molecular dynamics simulations of synaptic vesicle fusion I: a glimpse at the primed Synaptotagmin-SNARE-complexin complex
<p>Synaptic vesicles are primed into a state that is ready for fast neurotransmitter release upon Ca<sup>2+</sup>-binding to Syt1. This state likely includes trans-SNARE complexes between the vesicle and plasma membranes that are bound to Syt1 and complexins. However, the nature of this state and the steps leading to membrane fusion are unclear, in part because of the difficulty of studying this dynamic process experimentally. To shed light into these questions, we performed all-atom molecular dynamics simulations of systems containing trans-SNARE complexes between two flat bilayers or a vesicle and a flat bilayer with or without fragments of Syt1 and/or complexin-1. Our results need to be interpreted with caution because of the limited simulation times and the absence of key components, but suggest mechanistic features that may control release and help visualize potential states of the primed Syt1-SNARE-complexin-1 complex. In particular, the simulations suggest that SNAREs alone induce formation of extended membrane-membrane contact interfaces that may fuse slowly, and that the primed state contains macromolecular assemblies of trans-SNARE complexes bound to the Syt1 C<sub>2</sub>B domain and complexin-1 in a spring-loaded configuration that prevents premature membrane merger and formation of extended interfaces but keeps the system ready for fast fusion upon Ca<sup>2+</sup> influx.</p>
Molecular dynamics dataset of Synaptotagmin-1
<p>This dataset contains all-atom molecular dynamics trajectories of synaptotagmin-1 C2A (calcium free). Each trajectory is 2 µs long and the total cumulated simulation time is 184 µs. Details, including the molecular dynamics setup, are given in Hempel, T.; Plattner, N.; Noé, F. Coupling of Conformational Switches in Calcium Sensor Unraveled with Local Markov Models and Transfer Entropy. <em>J. Chem. Theory Comput.</em> <strong>2020</strong>, <em>16</em> (4), 2584–2593. <a href="https://doi.org/10.1021/acs.jctc.0c00043">https://doi.org/10.1021/acs.jctc.0c00043</a>.</p>
A lever hypothesis for Synaptotagmin-1 action in neurotransmitter release and Studies of Synaptotagmin-1 action by all-atom molecular dynamics simulations
Open the record for dataset details and reuse information.
All-atom molecular dynamics simulations of synaptic vesicle fusion I: a glimpse at the primed Synaptotagmin-SNARE-complexin complex
Open the record for dataset details and reuse information.
NMR data in 'Ca2+-dependent release of Synaptotagmin-1 from the SNARE complex on phosphatidylinositol 4,5-bisphosphate-containing membranes' by Voleti, Jaczynska and Rizo, eLife 2020
<p>The Ca<sup>2+</sup> sensor synaptotagmin-1 and the SNARE complex cooperate to trigger neurotransmitter release. Structural studies elucidated three distinct synaptotagmin-1-SNARE complex binding modes involving 'polybasic', 'primary' and 'tripartite' interfaces of synaptotagmin-1. We investigated these interactions using NMR and fluorescence spectroscopy. Synaptotagmin-1 binds to the SNARE complex through the polybasic and primary interfaces in solution. Ca<sup>2+</sup>-free synaptotagmin-1 binds to SNARE complexes anchored on PIP<sub>2</sub>-containing nanodiscs. R398Q/R399Q and E295A/Y338W mutations at the primary interface, which strongly impair neurotransmitter release, disrupt and enhance synaptotagmin-1-SNARE complex binding, respectively. Ca<sup>2+</sup> induces tight binding of synaptotagmin-1 to PIP<sub>2</sub>-containing nanodiscs, releasing synaptotagmin-1-SNARE interactions. Specific effects of mutations in the polybasic region on Ca<sup>2+</sup>-dependent synaptotagmin-1-PIP<sub>2</sub>-membrane interactions correlate with their effects on release. Our data suggest that synaptotagmin-1 binds to the SNARE complex through the primary interface and that Ca<sup>2+</sup> releases this interaction, inducing PIP<sub>2</sub>/membrane binding and allowing cooperation between synaptotagmin-1 and the SNAREs in membrane fusion to trigger release.</p>
NMR data in 'Ca2+-dependent release of Synaptotagmin-1 from the SNARE complex on phosphatidylinositol 4,5-bisphosphate-containing membranes' by Voleti, Jaczynska and Rizo, eLife 2020
Open the record for dataset details and reuse information.
Data from: Drosophila studies support a role for a presynaptic synaptotagmin mutation in a human congenital myasthenic syndrome
During chemical transmission, the function of synaptic proteins must be coordinated to efficiently release neurotransmitter. Synaptotagmin 2, the Ca2+ sensor for fast, synchronized neurotransmitter release at the human neuromuscular junction, has recently been implicated in a dominantly inherited congenital myasthenic syndrome associated with a non-progressive motor neuropathy. In one family, a proline residue within the C2B Ca2+-binding pocket of synaptotagmin is replaced by a leucine. The functional significance of this residue has not been investigated previously. Here we show that in silico modeling predicts disruption of the C2B Ca2+-binding pocket, and we examine the in vivo effects of the homologous mutation in Drosophila. When expressed in the absence of native synaptotagmin, this mutation is lethal, demonstrating for the first time that this residue plays a critical role in synaptotagmin function. To achieve expression similar to human patients, the mutation is expressed in flies carrying one copy of the wild type synaptotagmin gene. We now show that Drosophila carrying this mutation developed neurological and behavioral manifestations similar to those of human patients and provide insight into the mechanisms underlying these deficits. Our Drosophila studies support a role for this synaptotagmin point mutation in disease etiology.
Neurotransmitter release is triggered by a calcium-induced rearrangement in the Synaptotagmin-1/SNARE complex primary interface
Open the record for dataset details and reuse information.
Data from: Drosophila studies support a role for a presynaptic synaptotagmin mutation in a human congenital myasthenic syndrome
Open the record for dataset details and reuse information.
Synaptotagmin 2 is ectopically overexpressed in a widely used CaMK2a-Cre mouse line [T29-1 dataset]
GEO Series GSE179802. Mus musculus. 8 samples. Type: Expression profiling by high throughput sequencing.
Synaptotagmin-7 deficit causes insulin hypoactivity and contributes to behavioral alterations in mice
GEO Series GSE282863. Mus musculus. 13 samples. Type: Expression profiling by high throughput sequencing.
Synaptotagmin 2 is ectopically overexpressed in a widely used CaMK2a-Cre mouse line [CamiCre dataset]
GEO Series GSE179803. Mus musculus. 8 samples. Type: Expression profiling by high throughput sequencing.
Synaptotagmin 2 is ectopically overexpressed in a widely used CaMK2a-Cre mouse line
GEO Series GSE179804. Mus musculus. 16 samples. Type: Expression profiling by high throughput sequencing.
Data from: Synaptotagmin 7 functions as a Ca^2+ -sensor for synaptic vesicle replenishment
[No abstract entered]
Data from: Synaptotagmin 7 functions as a Ca^2+ -sensor for synaptic vesicle replenishment
Open the record for dataset details and reuse information.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.