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146 results for “Ca2+”
Adult-born granule cells modulate CA2 network activity during retrieval of developmental memories of the mother
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Chronic Ca2+ imaging of cortical neurons with long-term expression of GCaMP-X
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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>
Harnessing environmental Ca2+ for extracellular protein thermostabilization
<p>Ca<sup>2+</sup> is the third-most prevalent metal ion in the environment. EF hands are common Ca<sup>2+</sup>-binding motifs found in both extracellular and intracellular proteins of eukaryotes and prokaryotes. Cytoplasmic EF hand proteins often mediate allosteric control of signal transduction pathway components in response to intracellular Ca<sup>2+</sup> concentration fluctuations by coupling Ca<sup>2+</sup> binding to changes in protein structure. We show that an extracellular structural Ca<sup>2+</sup>-binding site mediates protein thermostabilization by such conformational coupling as well. Binding Ca<sup>2+</sup> to the EF hand of the extracellular (periplasmic) <i>Escherichia coli</i> glucose-galactose binding protein thermostabilizes this protein by ~17K relative to its Ca<sup>2+</sup>-free form. Using statistical thermodynamic analysis of a fluorescent conjugate of ecGGBP that reports simultaneously on ligand binding and multiple conformational states, we found that its Ca<sup>2+</sup>-mediated stabilization is determined by conformational coupling mechanisms in two independent conformational exchange reactions. Binding to folded and unfolded states determines the maximum Ca<sup>2+</sup>-mediated stability. A disorder®order transition accompanies formation of the Ca<sup>2+</sup> complex in the folded state and dictates the minimum Ca<sup>2+</sup> concentration at which the Ca<sup>2+</sup>-bound state becomes dominant. Similar transitions also encode the structural changes necessary for Ca<sup>2+</sup>-mediated control elements in signal transduction pathways. Ca<sup>2+</sup>-mediated thermostabilization and allosteric control therefore share a fundamental conformational coupling mechanism, which may have implications for the evolution of EF hands.</p>
Simulations of Na+ and Ca2+ binding to phospholipid membranes
<p>Simulations of various bilayers together with ions. A DOPC bilayer in the liquid disordered phase (310 K) and a DPPC bilayer in the gel phase (293 K), both formed of 200 lipids, were simulated with the presence of either 130 mM of NaCl or 450 mM of CaCl_2. The Slipids model [1–3] is employed for lipids, tip3p model for water, the ion parameters by Smith and Dang for NaCl [4] and the ion parameters by Kohagen et al. for CaCl_2 [5]. Trajectories with NaCl are 200 ns long, while with CaCl_2 they were either 500 ns (DOPC) or 800 ns (DPPC) long.</p> <p>Additionally, a ternary mixture of DPPC, DOPC, and cholesterol was simulated with the presence of 150 mM or 1 M of NaCl [4] at 310 K. The membrane was pre-assembled to contain Ld/Lo coexistence with a well-defined boundary. The Lo side consisted of 205 DPPC and 52 cholesterol molecules, while the Ld side consisted of 166 DOPC molecules. Trajectories are 200 ns long.</p> <p>The Slipids force field parameters are available at http://www.fos.su.se/~sasha/SLipids/ and the ion parameters are available at https://bitbucket.org/hseara/ions/<br> ––––––––––––––––––––––––––––––––––––––––––––––––––––––<br> The files are in GROMACS format. Trajectories (.xtc) are saved every 100 ps. Additionally, the final structure (.gro), topology (.top), index file (.ndx), energy output file (.edr), and binary run input files (for Gromacs 4.6->) (.tpr) are provided for each system. The common simulation parameter file except for the varying temperatures (md.mdp) is also provided.<br> ––––––––––––––––––––––––––––––––––––––––––––––––––––––<br> [1] Derivation and Systematic Validation of a Refined All-Atom Force Field for Phosphatidylcholine Lipids. Joakim P. M. Jämbeck and Alexander P. Lyubartsev, The Journal of Physical Chemistry B 2012 116 (10), 3164-3179, DOI: 10.1021/jp212503e</p> <p>[2] An Extension and Further Validation of an All-Atomistic Force Field for Biological Membranes. Joakim P. M. Jämbeck and Alexander P. Lyubartsev, Journal of Chemical Theory and Computation 2012 8 (8), 2938-2948, DOI: 10.1021/ct300342n</p> <p>[3] Another Piece of the Membrane Puzzle: Extending Slipids Further. Joakim P. M. Jämbeck and Alexander P. Lyubartsev, Journal of Chemical Theory and Computation 2013 9 (1), 774-784, DOI: 10.1021/ct300777p</p> <p>[4] Computer simulations of NaCl association in polarizable water. David E. Smith and Liem X. Dang, The Journal of Chemical Physics 1994 100, 3757-3766, DOI: 10.1063/1.466363</p> <p>[5] Accurate Description of Calcium Solvation in Concentrated Aqueous Solutions. Miriam Kohagen, Philip E. Mason, and Pavel Jungwirth, The Journal of Physical Chemistry B 2014 118 (28), 7902-7909, DOI: 10.1021/jp5005693</p>
A Trial of Anti-TNF Chimeric Monoclonal Antibody (cA2) in Korean Patients With Active Rheumatoid Arthritis Despite Methorexate (Extension Part)(Study P05645)(COMPLETED)
ClinicalTrials.gov study NCT00732875. IPD Sharing: YES. Countries: 0. Publications: 1.
Effect of Ca2+ Ionophore on Embryonic Development and Clinical Outcome in Cases With Previous Fertilization Arrest
ClinicalTrials.gov study NCT02683031. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.
How Secreted-embryo-derived Trypsin Initiates, Maintains and Terminates Ca2+ Signals in Uterine Epithelial Cells
ClinicalTrials.gov study NCT04865367. IPD Sharing: NO. Countries: 1. Publications: 15.
Choroidal Blood Flow Regulation During Isometric Exercise: Effects of Ca2+-Channel Blockade
ClinicalTrials.gov study NCT00280462. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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
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Data for: Inhibition of Ca2+-triggered secretion by hydrocarbon-stapled peptides
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Harnessing environmental Ca2+ for extracellular protein thermostabilization
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Data from Ca2+ mobilization-dependent reduction of the endoplasmic reticulum lumen is due to influx of cytosolic glutathione
<p>Research data associated with the manuscript "Ca2+ mobilization-dependent reduction of the endoplasmic reticulum lumen is due to influx of cytosolic glutathione" that is under consideration at BMC Biology.</p> <p>Data files are associated with eight main figures and four supplementary figures in the paper. For data reuse and file naming convention, note the read me.txt file.</p>
Data from: Enhanced store-operated Ca2+ influx and ORAI1 expression in ventricular fibroblasts from human failing heart
Excessive cardiac fibrosis, characterized by increased collagen-rich extracellular matrix (ECM) deposition, is a major predisposing factor for mechanical and electrical dysfunction in heart failure (HF). The human ventricular fibroblast (hVF) remodeling mechanisms that cause excessive collagen deposition in HF are unclear, although reports suggest a role for [Ca2+]i in fibrosis. Therefore, we determined the association of differences in cellular Ca2+ dynamics and collagen secretion/deposition between hVFs from failing and normal (control) hearts. Histology of left ventricle sections (Masson trichrome) confirmed excessive fibrosis in HF vs normal. In vitro, hVFs from HF showed increased secretion/deposition of soluble collagen in 48 hours of culture compared with control [85.9±7.4 μg/106 vs 58.5±8.8 μg/106 cells, P<0.05; (Sircol™ assay)]. However, collagen gene expressions (COL1A1 and COL1A2; rt-PCR) were not different. Ca2+ imaging (fluo-3) of isolated hVFs showed no difference in the thapsigargin-induced intracellular Ca2+ release capacity (control 16±1.4% vs HF 17±1.1%); however, Ca2+ influx via store-operated Ca2+ entry [SOCE /CRAC (Ca2+ release-activated)] channels was significantly (P≤0.05) greater in HF-hVFs (47±3%) compared with non-failing (35±5%). Immunoblotting for ICRAC channel components showed increased ORAI1 expression in HF-hVFs compared with normal without any difference in STIM1 expression. The Pearson's correlation coefficient for co-localization of STIM1/ORAI1 was significantly (P<0.01) greater in HF (0.5±0.01) than control (0.4±0.01) hVFs. The increase in collagen secretion of HF vs control hVFs was eliminated by incubation of hVFs with YM58483 (10 μM), a selective ICRAC inhibitor for 48 hours (66.78±5.87μg/106 cells vs 55.81±7.09 μg/106 cells, P=0.27). In conclusion, hVFs from HF have increased collagen secretion capacity vs non-failing hearts and this is related to increase in Ca2+ entry via SOCE and enhanced expression of ORAI, the pore-forming subunit. Therapeutic inhibition of SOCE may reduce the progression of cardiac fibrosis/HF.
Data from: Mechanism of Ca2+, Mg2+ and Fe3+ in fine cassiterite flotation using octanohydroxamic acid
The existence of metal ion should not be ignored in both hydrometallurgy and flotation. In this study, the effects of Ca2+, Mg2+ and Fe3+ on the flotation performance of cassiterite using octanohydroxamic acid (OHA) as the collector were investigated by the micro-flotation tests, X-ray photoelectron spectroscopy (XPS), fourier transform infrared spectroscopy (FTIR), contact angle, zeta (ζ) potential measurements and atomic force microscopy (AFM) imaging. The results of the flotation and contact angle experiments showed that the addition of Ca2+, Mg2+ and Fe3+ significantly decreased both the recovery and contact angle of cassiterite within pH ranged from 6.0 to 12.0 in the presence of OHA collector. ζ–potential measurements, solution chemistry analysis and FTIR measurements indicated that the flotation recovery of the cassiterite declined due to the CaOH+, MgOH+ and Fe(OH)3 sites on the cassiterite surface. XPS results indicated that the chemisorption of OHA on cassiterite surface and its adsorption combined with calcium ions effects finally changed the chemical properties of cassiterite surface. The AFM images also revealed that new species Fe(OH)3 of Fe3+ formed and adsorbed on the cassiterite surface at pH of 9.0. The adsorption of Fe(OH)3 reduced the adsorption of OHA on the cassiterite surface, thus the hydrophobicity of cassiterite was deteriorated.
Estimation of Ca2+ wet deposition in the Northern Hemisphere by use of CNN deep-learning model
<p>A dataset to estimate long-term and high-resolution gridded Ca2+ wet deposition across the Northern Hemisphere from 2001-2022.</p>
In-vivo two-photon imaging of aberrant Ca2+-waves following viral transduction of Ca2+ indicators in mice
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Association between Dysregulated Expression of Ca2+ and ROS-Related Gene Pairs and Breast Cancer Patient Survival
<p>This file is composed by two documents:</p> <ul> <li>Supplementary Table 1 containing an Excel file with data on gene expression, differential gene expression (tumoral versus normal), and survival outcomes related to redox (sheet 1) and calcium-related (sheet 2) genes.</li> <li>Suplementary Table 2 including a table summarizing the primary functions of selected redox- and calcium-related genes and various studies reporting their impact on breast cancer</li> </ul> <p>Both supplementary tables belongs to the study <strong><strong>Association between Dysregulated Expression of Ca2+ and ROS-Related Gene Pairs and Breast Cancer Patient Survival</strong></strong>, published in <strong>Molecular Diagnosis and therapy </strong></p>
Data from: Effects of rogue ryanodine receptors on Ca2+ sparks in cardiac myocytes
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Data from: Enhanced store-operated Ca2+ influx and ORAI1 expression in ventricular fibroblasts from human failing heart
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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.