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opencc-by-4.0Nov 2016View details →

OGD triggered Zn2+ rises and Ca2+ deregulation events in CA1 and CA3 hippocampal pyramidal neurons of MT-III and ZnT3 knockout mice.

The posted data provide the control characterization of the oxygen glucose deprivation (OGD) triggered occurrences of cytosolic Zn2+ rises and terminal Ca2+ deregulation events in individual CA1 and CA3 pyramidal neurons in acute hippocampal slices of the MT-III knockout mice ( 004649 - 129S7-Mt3tm1Rpa/J, Jackson Laboratory) and ZnT3 knockout mice ( 005064 - B6;129-Slc30a3tm1Rpa/J, Jackson Laboratory).

opencc-zeroJan 2024View details →

Impaired intracellular Ca2+ signaling contributes to age-related cerebral small vessel disease in Col4a1 mutant mice

Humans and mice with mutations in COL4A1 and COL4A2 manifest hallmarks of cerebral small vessel disease (cSVD). Mice with a missense mutation in Col4a1 at amino acid 1344 (Col4a1+/G1344D) exhibit age-dependent intracerebral hemorrhage (ICH) and brain lesions. Here we report that this pathology was associated with the loss of myogenic vasoconstriction, an intrinsic vascular response essential for the autoregulation of cerebral blood flow. Electrophysiological analyses showed that the loss of myogenic constriction resulted from blunted pressure-induced smooth muscle cell (SMC) membrane depolarization. Further, we found that dysregulation of membrane potential was associated with impaired Ca2+-dependent activation of large-conductance Ca2+-activated K+ (BK) and transient receptor potential melastatin 4 (TRPM4) cation channels linked to disruptions in sarcoplasmic reticulum (SR) Ca2+ signaling. Treating Col4a1+/G1344D mice with 4-phenylbutyrate, a compound that promotes the trafficking of misfolded proteins and alleviates SR stress, restored SR Ca2+ signaling and BK and TRPM4 channel activity, prevented loss of myogenic tone, and reduced ICH. We conclude that alterations in SR Ca2+ handling that impair membrane potential regulating ion channel activity result in dysregulation of SMC membrane potential and loss of myogenic tone contributing to age-related cSVD in Col4a1+/G1344D mice.

opencc-by-4.0Aug 2022View details →

Source data for "Ca2+ channels couple spiking to mitochondrial metabolism in substantia nigra dopaminergic neurons"

Fig.1Aa-c.tif 2PLSM images (Fura-2 filled neuron) used for the reconstruction in Fig.1A   Fig1CDJ.xlsx Numerical data for the charts in Fig. 1C, Fig.1D, Fig.1J   Fig.1F_GCEPIA1er.tif Confocal image (green channel, G-CEPIA1er) for Fig. 1F   Fig.1F_TH.tif Confocal image (blue channel, anti-TH immunostaining) for Fig. 1F   Fig.1G_GCEPIA1er.tif Confocal image (green channel, G-CEPIA1er) for Fig. 1G   Fig.1G_CRT.tif Confocal image (magenta channel, anti-CRT immunostaining) for Fig. 1G   Fig.1H_GCEPIA1er.tif Confocal image (green channel, G-CEPIA1er) for Fig. 1H   Fig.1H_TH.tif Confocal image (blue channel, anti-TH immunostaining) for Fig. 1H   Fig. 2B_mitoGCaMP6.tif Confocal image (green channel, mito-GCaMP6) for Fig. 2B   Fig.2B_TH.tif Confocal image (blue channel, anti-TH immunostaining) for Fig. 2B   Fig. 2C_mitoGCaMP6.tif Confocal image (green channel, mito-GCaMP6) for Fig. 2C   Fig.2C_COXIV.tif Confocal image (magenta channel, anti-COXIV immunostaining) for Fig. 2C   Fig. 2D_mitoGCaMP6.tif Confocal image (green channel, mito-GCaMP6) for Fig. 2D   Fig.2D_TH.tif Confocal image (blue channel, anti-TH immunostaining) for Fig. 2D   Fig.2FGJL.xlsx Numerical data for the charts in Fig. 2F, Fig.2G, Fig.2J, Fig.2L   Fig.3BDE.xlsx Numerical data for the charts in Fig. 3B, Fig.3D, Fig.3E   Fig.3C_Alexa.tif MAX Projection of z-stack of 2PLSM images (magenta channel, Alexa 594 dye) used to generate Fig.3C top panel   Fig.3C_mitoGCaMP6.tif MAX Projection of z-stack of 2PLSM images (green channel, mito-GCaMP6) used to generate Fig.3C top panel   Fig.3C_inset_dendritic_mitoGCaMP6.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.3C bottom left panel   Fig.3C_inset_soma_mitoGCaMP6.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.3C bottom right panel   Fig. 4A_PercevalHR.tif Confocal image (green channel, PercevalHR) for Fig.4A   Fig.4A_TH.tif Confocal image (blue channel, anti-TH immunostaining) for Fig.4A   Fig. 4B_PercevalHR.tif Confocal image (green channel, PercevalHR) for Fig.4B   Fig.4B_TH.tif Confocal image (blue channel, anti-TH immunostaining) for Fig.4B   Fig.4G.xlsx Numerical data for the charts in Fig.4G   Fig.5BDFHI.xlsx Numerical data for the charts in Fig.5B, Fig.5D, Fig.5F, Fig.5H, Fig.5I   Fig.6ADEFJKLN.xlsx Numerical data for the charts in Fig.6A, Fig.6D, Fig.6E, Fig.6F, Fig.6J, Fig.6K, Fig.6L, Fig.6N   Fig.6H_mitoroGFP.tif 2PLSM image (green channel, mito-roGFP) for Fig.6H   Fig.6M_MCU-KO.tif Combined EM micrographs used to generate Fig. 6M right side   Fig.6M_wildtype.tif Combined EM micrographs used to generate Fig. 6M left side   Fig.7CEFG.xlsx Numerical data for the charts in Fig.7C, Fig.7E, Fig.7F, Fig.7G   Fig.8CEHJK.xlsx Numerical data for the charts in Fig.8C, Fig.8E, Fig.8H, Fig.8J, Fig.8K   Fig.S1A_bottom.tif 2PLSM image (green channel, G-CEPIA1er) for Fig.S1A bottom panel (low Ca2+)   Fig.S1A_top.tif 2PLSM image (green channel, G-CEPIA1er) for Fig.S1A top panel (high Ca2+)   Fig.S1B.xlsx Numerical data for the chart in Fig.S1B   Fig.S2A_baseline.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2A middle panel (baseline)   Fig.S2A_MAX.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2A top panel (high Ca2+)   Fig.S2A_min.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2A bottom panel (low Ca2+)   Fig.S2C_baseline.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2C middle panel (baseline)   Fig.S2C_MAX.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2C top panel (high Ca2+)   Fig.S2C_min.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2C bottom panel (low Ca2+)   Fig.S2E_baseline.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2E bottom left panel (baseline)   Fig.S2E_end.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2E bottom right panel   Fig.S2E_peak.tif 2PLSM image (green channel, mito-GCaMP6) for Fig.S2E bottom center panel   Fig.S2F.xlsx Numerical data for the chart in Fig.S2F   Fig.S3ABC.xlsx Numerical data for the charts in Fig.S3A, Fig.S3B, Fig.S3C   Fig.S4CD.xlsx Numerical data for the charts in Fig.S4C, Fig.S4D   Fig.S5ABC.xlsx Numerical data for the charts in Fig.S5A, Fig.S5B, Fig.S5C   Fig.S7A.tif 2PLSM image (green channel, GCaMP6) for Fig.S7A   Fig.S7CEFGH.xlsx Numerical data for the charts in Fig.S7C, Fig.S7E, Fig.S7F, Fig.S7G, Fig.S7H   Fig.S8ABCDEF.xlsx Numerical data for the charts in Fig.S8A, Fig.S8B, Fig.S8C, Fig.S8D, Fig.S8E, Fig.S8F   Fig.S9AHIJK.xlsx Numerical data for the charts in Fig.S9A, Fig.S9H, Fig.S9I, Fig.S9J, Fig.S9K   Fig.S9B_wildtype_DLStr.tif Confocal image of dorso-laterateral striatum in wildtype mouse (red channel, anti-TH immunostaining) for Fig.S9B   Fig.S9C_MCU-KO_DLStr.tif Confocal image of dorso-laterateral striatum in MCU-KO mouse (red channel, anti-TH immunostaining) for Fig.S9C   Fig.S9D_wildtype_SN.tif Confocal image of midbrain in wildtype mouse (red channel, anti-TH immunostaining) for Fig.S9D   Fig.S9E_MCU-KO_SN.tif Confocal image of midbrain in MCU-KO mouse (red channel, anti-TH immunostaining) for Fig.S9E   Fig.S9F_wildtype_openfield.png Open field path tracked for wildtype mouse for Fig.S9F   Fig.S9G_MCU-KO_openfield.png Open field path tracked for MCU-KO mouse for Fig.S9G   Fig.S10A.xlsx Numerical data for the charts in Fig.S10A

MD simulation trajectory of a POPC/POPS (4:1) bilayer with 715mM CaCl2, Berger force field for lipids, scaled charges for Ca2+ and Cl-

MD simulation trajectory of a POPC/POPS (4:1) bilayer with 715 mM CaCl2 (104 POPC, 24 POPS, 26 POPS, 4306 WAT, 72 Ca2+, 112 Cl-). Additional Ca2+ cations added to neutralize the negative charge of POPS (leading to total Ca2+ concentration of 919 mM). Berger force field for lipids, scaled charges employed for calcium and chloride ions. Gromacs 4.5.5, T=310K, 300 ns trajectories were calculated with the last 100 ns stored here. Used in (see therein also a detailed description of ion scaling): A. Melcrova, S. Pokorna, S. Pullanchery, M. Kohagen, P. Jurkiewicz, M. Hof, P. Jungwirth, P. S. Cremer, L. Cwiklik, The complex nature of calcium cation interactions with phospholipid bilayers Scientific Reports 2016, 6, 38035. DOI: 10.1038/srep38035

MD simulation trajectory of a POPC bilayer with 716mM CaCl2, Berger force field for lipids, scaled charges for Ca2+ and Cl-

MD simulation trajectory of a POPC bilayer with 716 mM CaCl2 (128 POPC, 26 POPS, 4308 WAT, 56 Ca2+, 112 Cl-). Berger force field for lipids, scaled charges employed for calcium and chloride ions. Gromacs 4.5.5, T=310K, 200 ns trajectories were calculated with the last 100 ns stored here. Used in (see therein also a detailed description of ion scaling): A. Melcrova, S. Pokorna, S. Pullanchery, M. Kohagen, P. Jurkiewicz, M. Hof, P. Jungwirth, P. S. Cremer, L. Cwiklik, The complex nature of calcium cation interactions with phospholipid bilayers Scientific Reports 2016, 6, 38035. DOI: 10.1038/srep38035

MD simulation trajectory of a POPC/POPS (4:1) bilayer with 102mM CaCl2, Berger force field for lipids, scaled charges for Ca2+ and Cl-

MD simulation trajectory of a POPC/POPS (4:1) bilayer with 102 mM CaCl2 (104 POPC, 24 POPS, 26 POPS, 4306 WAT, 24 Ca2+, 16 Cl-). Additional Ca2+ cations added to neutralize the negative charge of POPS (leading to total Ca2+ concentration of 306 mM). Berger force field for lipids, scaled charges employed for calcium and chloride ions. Gromacs 4.5.5, T=310K, 300 ns trajectories were calculated with the last 100 ns stored here. Used in (see therein also a detailed description of ion scaling): A. Melcrova, S. Pokorna, S. Pullanchery, M. Kohagen, P. Jurkiewicz, M. Hof, P. Jungwirth, P. S. Cremer, L. Cwiklik, The complex nature of calcium cation interactions with phospholipid bilayers Scientific Reports 2016, 6, 38035. DOI: 10.1038/srep38035

MD simulation trajectory of a POPC bilayer with 100mM CaCl2, Berger force field for lipids, scaled charges for Ca2+ and Cl-

MD simulation trajectory of a POPC bilayer with 100 mM CaCl2 (128 POPC, 26 POPS, 4452 WAT, 8 Ca2+, 16 Cl-). Berger force field for lipids, scaled charges employed for calcium and chloride ions. Gromacs 4.5.5, T=310K, 200 ns trajectories were calculated with the last 100 ns stored here). Used in (see therein also a detailed description of ion scaling): A. Melcrova, S. Pokorna, S. Pullanchery, M. Kohagen, P. Jurkiewicz, M. Hof, P. Jungwirth, P. S. Cremer, L. Cwiklik, The complex nature of calcium cation interactions with phospholipid bilayers Scientific Reports 2016, 6, 38035. DOI: 10.1038/srep38035

opencc-by-4.0May 2024View details →

General dataset of PNAS article " Ca2+ permeation through C-terminal cleaved, but not full-length human Pannexin1 hemichannels, mediates cell death"

This repository contains an extended version of all real-time dye uptake evaluations, Ca2+ signal measurements, microscopic and gel images, and the corresponding statistical analyzes for each graph presented in the associated article.

opencc-by-4.0May 2018View details →

Ano4 as a Ca2+ dependent cation channel

Figure 1, Figure 2, Figure 3, Figure 4, Figure 5 Supp (Supplemental information 1-7) 2nd revision

opencc-zeroNov 2022View details →

Chronic Ca2+ imaging of cortical neurons with long-term expression of GCaMP-X

Dynamic Ca2+ signals reflect acute changes in membrane excitability and also mediate signaling cascades in chronic processes. In both cases, chronic Ca2+ imaging is often desired but challenged by the cytotoxicity intrinsic to calmodulin (CaM)-based GCaMP, a series of genetically-encoded Ca2+ indicators that have been widely applied. Here, we demonstrate the performance of GCaMP-X in chronic Ca2+ imaging of cortical neurons, where GCaMP-X by design is to eliminate the unwanted interactions between the conventional GCaMP and endogenous (apo)CaM-binding proteins. By expressing in adult mice at high levels over an extended time frame, GCaMP-X showed less damage and improved performance in two-photon imaging of sensory (whisker-deflection) responses or spontaneous Ca2+ fluctuations, in comparison with GCaMP. Chronic Ca2+ imaging of one month or longer was conducted for cultured cortical neurons expressing GCaMP-X, unveiling that spontaneous/local Ca2+ transients progressively developed into autonomous/global Ca2+ oscillations. Along with the morphological indices of neurite length and soma size, the major metrics of oscillatory Ca2+, including rate, amplitude and synchrony were also examined. Dysregulations of both neuritogenesis and Ca2+ oscillations became discernible around 2–3 weeks after virus injection or drug induction to express GCaMP in newborn or mature neurons, which were exacerbated by stronger or prolonged expression of GCaMP. In contrast, neurons expressing GCaMP-X were significantly less damaged or perturbed, altogether highlighting the unique importance of oscillatory Ca2+ to neural development and neuronal health. In summary, GCaMP-X provides a viable solution for Ca2+ imaging applications involving long-time and/or high-level expression of Ca2+ probes.

opencc-by-4.0Jul 2023View details →

Ca2+ imaging data for: A rigidity transition of MEC-2/Stomatin condensates controls neuronal mechanotransduction during touch sensing

Calcium imaging data from Sanfeliu et al, NCB, 2023. Project contains fluorescence data to characterize the activity of the touch receptor neurons (TRNs) - which are mechanically activated upon touch – in the model organism Caenorhabditis elegans. The set of data includes wild-type animals as a reference and two different mutants to understand their role during touch sensation: MEC-2(R385H) and UNC-89 knock-out.

opencc-by-4.0Oct 2022View details →

Light-induced nanoscale deformation in azobenzene thin film triggers rapid intracellular Ca2+ increase via mechanosensitive cation channels

This dataset contains raw data for a research article: material characterization data of Disperse Red 1 glass, calcium imaging data of Madin Darby Canine Kidney II epithelial cells that express the genetic calcium indicator jRCaMP1b and immunofluorescence stainings of Piezo1-channels and the actin cytoskeleton in the same cell line. Light induced material deformations were conducted with Zeiss LSM 780 confocal microscope with 488 nm wavelength excitation. The generated topographies were analyzed with atomic force microscopy (AFM) and digital holographic microscopy (DHM), and particle image velocimetry (PIV) was used to determine lateral deformations. Calcium imaging was conducted with the same microscope with 561 nm excitation and calcium signals were recorded in response to light induced material deformations (stimulation performed after 10 frames) (Zeiss C Apo 63x/1.20 objective, pixel size 200 nm, frame rate 1.23 sec/fame, channel1: fluorescence emission, channel2: brightfield). Apical stimulations were conducted with Nikon Eclipse FN1 utilizing micromanipulation (pixel size 200 nm, NIR Apo 40x 0.8W DIC N2 objective). Immunofluorescence stainings (in normal conditions (channel1: nuclei, channel2: Piezo1, channel3: jRCaMP1b, channel4: actin) or after cytochalainD treatment showing actin cytoskeleton depolymerization (channel1: nuclei, channel2: ZO1, channel3: jRCaMP1b, channel4: actin)) were imaged with Nikon A1R (SR Apo TIRF 100x/1.49 objective, pixel size 40 nm, Z-step to 99 nm, deconvolution with Huygens Essential)

publicAug 2024View details →

Data for: Mitochondrial Ca2+-coupled generation of reactive oxygen species, peroxynitrite formation, and endothelial dysfunction in Cantú syndrome

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publicDec 2024View details →

Data from: Cytosolic S100A8/A9 promotes Ca2+ supply at LFA-1 adhesion clusters during neutrophil recruitment

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publicMay 2025View details →

Mechanism of Ca2+ in regulating pupation defects of Bombyx mori after exposure to chlorantraniliprole

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publicJan 2024View details →

Impaired intracellular Ca2+ signaling contributes to age-related cerebral small vessel disease in Col4a1 mutant mice

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