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523 results for “cell migration”
( R, S)-Equol 7-β-D-glucuronide, but not other circulating isoflavone metabolites, modulates migration and tubulogenesis in human aortic endothelial cells targeting the VEGF pathway
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tRNA-derived fragment tRF-Glu49 inhibits cell proliferation, migration and invasion in cervical cancer by targeting FGL1
<p>A transfer RNA (tRNA)-derived fragment was found to be a new possible biological marker and target in carcinoma therapy. However, the effect exerted by tRFs on cervical carcinoma is still unclear. We identify the potential tumor suppressor gene tRF-Glu49 in cervical carcinoma through tRF and ti-RNA microarray investigation. We then demonstrated that tRF-Glu49 showed downregulation within the cervical carcinoma tissue and was associated with less aggressive clinical features and a better prognosis. Phenotypic studies revealed that tRF-Glu49 inhibited cervical cell proliferation, migration, and invasion processes. Mechanistic investigation revealed that tRF-Glu49 directly regulated the oncogene, fibrinogen-like protein-1 (FGL1). In general, according to the result achieved in this study, tRF-Glu49 can modulate cervical cell proliferation, migration, and invasion processes through the target process for FGL1, and tRF-Glu49 is likely to be a possible prognostic biological marker in patients with cervical carcinoma.</p>
Data from: T cell morphodynamics reveal periodic shape oscillations in 3D migration
<p>Surface segmentation data of cytotoxic T cells migrating in 3D collagen matrices, imaged by lattice light-sheet microscopy and used for quantitative morphodynamic analysis in the manuscript: T Cell Morphodynamics Reveal Periodic Shape Oscillations in 3D Migration.</p>
NSD3-Short Promotes Migration of A549 Lung Cancer Cells
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp025 Objective:</strong> In a previous experiment (exp024), we observed an increase in E-cadherin expression in response to knockdown of the short isoform of NSD3. To determine if this change is functionally relevant, we performed wound healing assays to measure any corresponding alteration in the migratory potential of A549 lung epithelial cancer cells.</p>
Data from: Cell proliferation and migration during early development of a symbiotic scleractinian coral
In scleractinian reef-building corals, patterns of cell self-renewal, migration and death remain virtually unknown, limiting our understanding of cellular mechanisms underlying initiation of calcification, and ontogenesis of the endosymbiotic dinoflagellate relationship. In this study we pulse-labeled the coral Stylophora pistillata for 24 h with BrdU at four life stages (planula, early metamorphosis, primary polyp, and adult colony) to investigate coral and endosymbiont cell proliferation during development, while simultaneously recording TUNEL-positive, i.e. apoptotic, nuclei. In the primary polyp, the fate of BrdU-labeled cells was tracked during a 3 days chase. The pharynx and gastrodermis were identified as the most proliferative tissues in the developing polyp, and BrdU-labeled cells accumulated in the surface pseudostratified epithelium and the skeletogenic calicodermis during the chase, revealing cell migration to these epithelia. Surprisingly, the lowest cell turnover was recorded in the calicodermis at all stages, despite active, ongoing skeletal deposition. In dinoflagellate symbionts, DNA synthesis was systematically higher than in coral host gastrodermis, especially in planula and early metamorphosis. The symbiont to host cell ratio remained however constant, indicating successive post-mitotic control mechanisms by the host of its dinoflagellate density in early life stages, increasingly shifting to apoptosis in the growing primary polyp.
miRNA149 as candidate for facial clefting and neural crest cell migration: Appendix data
<p>Appendix Data for the paper "<strong>miRNA149 as candidate for facial clefting and neural crest cell migration</strong>" by Stüssel et al.</p> <p>Appendix Table S1: Overview of candidate microRNAs expressed in human neural crest cells</p> <p>Appendix Table S2: nsCL/P associated candidate variants colocalizing with candidate miRNAs</p> <p>Appendix Table S3: Overview of Differentially Expressed genes</p> <p>Appendix Table S4: Overview of GO-gene sets enriched in pathway analysis</p> <p>Appendix Table S5: GO-Terms of pathway enrichment analysis with term-level 5 and group size <100</p>
hERG Kv11.1 and Janus Kinase 2 interplay in retinoblastoma cell migration
<p>Docking poses, Molecular Dynamics simulation starting structures and MD trajectories</p>
Movie S2. T-cell migration in a 5 dpf dock11-knockout zebrafish embryo
<p>Representative time-lapse confocal microscopy movie showing the migration of fluorescently labeled T cells in the region around the thymus (anterior region) in a 5 days postfertilization (dpf) <em>dock11</em>-knockout <em>lck:nlsmCherry </em>transgenic zebrafish embryo<em>. </em>Lines correspond to the trajectories of the movement over time of Lck-positive T‑cell progenitors.</p> <p>This movie corresponds to Movie S2 from Supplementary Appendix of Block et al., Systemic Inflammation and Normocytic Anemia in DOCK11 Deficiency. N Engl J Med 2023.</p>
Movie S1. T cell migration in a 5 dpf control zebrafish embryo
<p>Representative time-lapse confocal microscopy movie showing the migration of fluorescently labeled T cells in the region around the thymus (anterior region) in a 5 days postfertilization (dpf) control <em>lck:nlsmCherry </em>transgenic zebrafish embryo<em>. </em>Lines correspond to the trajectories of the movement over time of Lck-positive T-cell progenitors.</p> <p>This movie corresponds to Movie S1 from Supplementary Appendix of Block et al., Systemic Inflammation and Normocytic Anemia in DOCK11 Deficiency. N Engl J Med 2023.</p>
Data and code for "Migration and division in cell monolayers on substrates with topological defects"
<p>Raw data for experiment (experiment.zip) and basic simulation code (simulation.zip) for the paper "Migration and division in cell monolayers on substrates with topological defects"</p>
Data from: Cell proliferation and migration during early development of a symbiotic scleractinian coral
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Data from: Ovarian BDNF promotes survival, migration, and attachment of tumor precursors originated from p53 mutant fallopian tube epithelial cells
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Data from: T cell morphodynamics reveal periodic shape oscillations in 3D migration
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Data from: Reduced CTGF Expression Promotes Cell Growth, Migration, and Invasion in Nasopharyngeal Carcinoma
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Data: Size-dependent patterns of cell proliferation and migration in freely-expanding epithelia
<p>Raw images ('*.tif" file extensions) and core measurement files ('*.mat file extension). For small and large circles, we include images of phase, GFP, RFP, and nuclei. We also include two ellipses in phase. '<a href="https://zenodo.org/api/files/f94dc36b-aa3a-40f5-800a-035282fdfad7/t0SummaryStats.mat">t0SummaryStats.mat</a>' gives information for the starting conditions of tissues represented by the '<a href="https://zenodo.org/api/files/f94dc36b-aa3a-40f5-800a-035282fdfad7/PIVunsmoothed.mat">PIVunsmoothed.mat</a>' and '<a href="https://zenodo.org/api/files/f94dc36b-aa3a-40f5-800a-035282fdfad7/Kymographs.mat">Kymographs.mat</a>' datasets. '<a href="https://zenodo.org/api/files/f94dc36b-aa3a-40f5-800a-035282fdfad7/ContinuityEqn_FVM.m">ContinuityEqn_FVM.m</a>' includes the solution to the continuity equation via the finite volume method as detailed in the materials and methods, and relies on data in '<a href="https://zenodo.org/api/files/f94dc36b-aa3a-40f5-800a-035282fdfad7/Kymographs.mat">Kymographs.mat</a>' and '<a href="https://zenodo.org/api/files/f94dc36b-aa3a-40f5-800a-035282fdfad7/t0SummaryStats_continuityEqn.mat">t0SummaryStats_continuityEqn.mat</a>'.</p>
Cancer cells optimize elasticity for efficient migration
<p>Cancer progression is associated with alternations in the cytoskeletal architecture of cells and, consequently, their mechanical properties such as stiffness. Changing the mechanics of cells enables cancer cells to migrate and invade to distant organ sites. This process, metastasis, is the main reason for cancer-related mortality. Cell migration is an essential step toward increasing the invasive potential of cells. Although many studies have shown that the migratory speed and the invasion of cells can be inversely correlated to the stiffness of cells, some other investigations indicate exactly opposing results. In the current work, based on the strain energy stored in cells due to the contractile forces, we defined an energy-dependent term, migratory index, to approximate how changes in the mechanical properties of cells influence cell migration required for cancer progression. Cell migration involves both cell deformation and force transmission within cells. The effects of these two parameters can be represented equally by the migratory index. Our mechanical modeling and computational study show that cells depending on their shape, size, and other physical parameters, have a maximum migratory index taking place at a specific range of cell bulk stiffness, indicating the most favorable conditions for invasive mobility. This approximate model can be used to explain why the stiffness of cells varies during cancer progression. We believe that the stiffness of invasive cells depending on the stiffness of their non-invasive counterparts is either decreased or increased to reach the critical condition in which the mobility potential of cells is approximated to be maximum.</p>
Quantifying monolayer cell migration sample dataset
<p>The sample data to use with the Quantifying monolayer cell migration chapter of the 'Bioimage Data Analysis Workflows - Advanced Components and Methods' Neubias textbook.</p>
Crosstalk between Mast Cells and Lung Fibroblasts Is Modified by Alveolar Extracellular Matrix and Influences Epithelial Migration
<p>Datasets for the data generated and presented in the article: https://doi.org/10.3390/ijms22020506</p>
Data from: Cell migration through three-dimensional confining pores: speed accelerations by deformation and recoil of the nucleus
Directional cell migration in dense three-dimensional (3D) environments critically depends upon shape adaptation and is impeded depending on the size and rigidity of the nucleus. Accordingly, the nucleus is primarily understood as a physical obstacle, however, its pro-migratory functions by step-wise deformation and reshaping remain unclear. Using atomic force spectroscopy, time-lapse fluorescence microscopy and shape change analysis tools, we determined nuclear size, deformability, morphology and shape change of HT1080 fibrosarcoma cells expressing the Fucci cell cycle indicator or being pre-treated with chromatin-decondensating agent TSA. We show oscillating peak accelerations during migration through 3D collagen matrices and microdevices that occur during shape reversion of deformed nuclei (recoil), and increase with confinement. During G1 cell cycle phase, nucleus stiffness was increased and yielded further increased speed fluctuations together with sustained cell migration rates in confinement as compared to interphase populations, or to periods of intrinsic nuclear softening in the S/G2 cell cycle phase. Likewise, nuclear softening by pharmacological chromatin decondensation or after lamin A/C depletion reduced peak oscillations in confinement. In conclusion, deformation and recoil of the stiff nucleus contributes to saltatory locomotion in dense tissues.
Data from: The core planar cell polarity gene, Vangl2, directs adult corneal epithelial cell alignment and migration
This study shows that the core planar cell polarity (PCP) genes direct the aligned cell migration in the adult corneal epithelium, a stratified squamous epithelium on the outer surface of the vertebrate eye. Expression of multiple core PCP genes was demonstrated in the adult corneal epithelium. PCP components were manipulated genetically and pharmacologically in human and mouse corneal epithelial cells in vivo and in vitro. Knockdown of VANGL2 reduced the directional component of migration of human corneal epithelial (HCE) cells without affecting speed. It was shown that signalling through PCP mediators, dishevelled, dishevelled-associated activator of morphogenesis and Rho-associated protein kinase directs the alignment of HCE cells by affecting cytoskeletal reorganization. Cells in which VANGL2 was disrupted tended to misalign on grooved surfaces and migrate across, rather than parallel to the grooves. Adult corneal epithelial cells in which Vangl2 had been conditionally deleted showed a reduced rate of wound-healing migration. Conditional deletion of Vangl2 in the mouse corneal epithelium ablated the normal highly stereotyped patterns of centripetal cell migration in vivo from the periphery (limbus) to the centre of the cornea. Corneal opacity owing to chronic wounding is a major cause of degenerative blindness across the world, and this study shows that Vangl2 activity is required for directional corneal epithelial migration.
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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.