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201 results for “Cell Adhesion”
Patient-derived and artificial ascites have minor effects on MeT-5A mesothelial cells and do not facilitate ovarian cancer cell adhesion
<p>Raw data of "Patient-derived and artificial ascites have minor effects on MeT-5A mesothelial cells and do not facilitate ovarian cancer cell adhesion".</p>
Рис. 7. Варианты преΑсказанной Αоменной структуры моΛекуΛ аΑгезии гемоцитов моΛΛюсков Planorbarius corneus. УсΛовные обозначения и сокращения: 1–3 — β-интегрины, 4–5 — α-интегрины, 6–7 — сеΛектины, 8–11 — моΛекуΛы семейства САМ (сell adhesiom molecues), INB — субъеΑиницы β-интегрина, IntegrinBcyt — цитопΛазматический Αомен β-интегрина, CY — цистатинопоΑобный Αомен, Int alpha — Αомен α-интегрина, FN3 — Αомен фибронектина типа 3, CCP — Αомен контроΛя компΛемента Fig. 7. Variants of the predicted domain structure of adhesion molecules from hemocytes of Planorbarius corneus molluscs. Symbols and abbreviations: 1–3 — β-integrins, 4–5 — α–integrins, 6–7 — selectins, 8–11 — molecules of the СAM family (cell adhesion molecules), INB — β-integrin subunits, IntegrinBcyt — cytoplasmic domain of β-integrin, CY — cystatin-like domain, Int alpha — α-integrin domain, FN3 — fibronectin type 3 domain, CCP — complement control protein domain in Pathogen recognition molecules from hemocytes of Planorbarius corneus molluscs (Planorbidae, Pulmonata)
Рис. 7. Варианты преΑсказанной Αоменной структуры моΛекуΛ аΑгезии гемоцитов моΛΛюсков Planorbarius corneus. УсΛовные обозначения и сокращения: 1–3 — β-интегрины, 4–5 — α-интегрины, 6–7 — сеΛектины, 8–11 — моΛекуΛы семейства САМ (сell adhesiom molecues), INB — субъеΑиницы β-интегрина, IntegrinBcyt — цитопΛазматический Αомен β-интегрина, CY — цистатинопоΑобный Αомен, Int alpha — Αомен α-интегрина, FN3 — Αомен фибронектина типа 3, CCP — Αомен контроΛя компΛемента Fig. 7. Variants of the predicted domain structure of adhesion molecules from hemocytes of Planorbarius corneus molluscs. Symbols and abbreviations: 1–3 — β-integrins, 4–5 — α–integrins, 6–7 — selectins, 8–11 — molecules of the СAM family (cell adhesion molecules), INB — β-integrin subunits, IntegrinBcyt — cytoplasmic domain of β-integrin, CY — cystatin-like domain, Int alpha — α-integrin domain, FN3 — fibronectin type 3 domain, CCP — complement control protein domain
The cell adhesion molecule Sdk1 shapes assembly of a retinal circuit that detects localized edges
<p>Nearly 50 different mouse retinal ganglion cell (RGC) types sample the visual scene for distinct features. RGC feature selectivity arises from its synapses with a specific subset of amacrine (AC) and bipolar cell (BC) types, but how RGC dendrites arborize and collect input from these specific subsets remains poorly understood. Here we examine the hypothesis that RGCs employ molecular recognition systems to meet this challenge. By combining calcium imaging and type-specific histological stains we define a family of circuits that express the recognition molecule Sidekick 1 (Sdk1) which include a novel RGC type (S1-RGC) that responds to local edges. Genetic and physiological studies revealed that Sdk1 loss selectively disrupts S1-RGC visual responses which result from a loss of excitatory and inhibitory inputs and selective dendritic deficits on this neuron. We conclude that Sdk1 shapes dendrite growth and wiring to help S1-RGCs become feature selective.</p>
A multiscale theory for spreading and migration of adhesion-reinforced mesenchymal cells
<p>We present a chemomechanical whole-cell theory for the spreading and migration dynamics of mesenchymal cells that can actively reinforce their adhesion to an underlying viscoelastic substrate as a function of its stiffness. Our multiscale model couples the adhesion reinforcement effect at the subcellular scale with the nonlinear mechanics of the nucleus-cytoskeletal network complex at the cellular scale to explain the concurrent monotonic area-stiffness and non-monotonic speed-stiffness relationships observed in experiments: We consider that large cell spreading on stiff substrates flattens the nucleus, increasing the viscous drag force on it. The resulting force balance dictates a reduction in the migration speed on stiff substrates. We also reproduce the experimental influence of the substrate viscosity on the cell spreading area and migration speed by elucidating how the viscosity may either maintain adhesion reinforcement or prevent it depending on the substrate stiffness. Additionally, our model captures the experimental directed migration behavior of the adhesion-reinforced cells along a stiffness gradient, known as durotaxis, as well as up or down a viscosity gradient (viscotaxis or anti-viscotaxis), the cell moving towards an optimal viscosity in either case. Overall, our theory explains the intertwined mechanics of the cell spreading, migration speed and direction in the presence of the molecular adhesion reinforcement mechanism. </p>
Data from: ESCRT-III-dependent adhesive and mechanical changes are triggered by a mechanism detecting alteration of Septate Junction integrity in Drosophila epithelial cells
<p><span>Barrier functions of proliferative epithelia are constantly challenged by mechanical and chemical constraints. How epithelia respond to and cope with disturbances of barrier functions to allow tissue integrity maintenance is poorly characterized. Cellular junctions play an important role in this process and intracellular traffic contribute to their homeostasis. Here, we reveal that, in <em>Drosophila</em> pupal <em>notum</em>, alteration of the bi- or tricellular septate junctions (SJs) triggers a mechanism with two prominent outcomes. On one hand, there is an increase in the levels of E-cadherin, F-Actin and non-muscle Myosin II in the plane of adherens junctions. On </span><span>the other hand, β-integrin/Vinculin-positive cell contacts are reinforced along the lateral and basal membranes. We found that the weakening of SJ integrity, caused by the depletion of bi- or tricellular SJ components, alters ESCRT-III/Vps32/Shrub distribution, reduces degradation, and instead favours recycling of SJ components, an effect that extends to other recycled transmembrane protein cargoes including Crumbs, its effector β-Heavy Spectrin</span><span> Karst, and </span><span>β-integrin</span><span>. We propose a mechanism by which epithelial cells, upon sensing alterations of the septate junction</span><span>,</span><span> reroute the function of Shrub to adjust the balance of degradation/recycling of junctional cargoes and thereby compensate for barrier junction defects to maintain epithelial integrity.</span></p>
Effect of heterogeneous substrate adhesivity of follower cells on speed and tension profile of leader cells in primary keratocyte collective cell migration
<p><span>In single keratocyte motility, membrane tension is reported to be high at cell-fronts and believed to establish front coherence. To understand role of membrane mechanics in collective cell migration, we study membrane height fluctuations in cell sheets from fish scales using interference reflection microscopy (IRM). We report the monolayer to have cells lacking substrate adhesion and show that such "non-sticky" cells can form bridges between leader cells and far-away follower cells. Do such interactions alter motility and membrane mechanics in such leaders? We find non-significant, but reduced speed for leaders with "non-sticky" followers in comparison to other leaders. Cells show high phenotypic variability in their membrane fluctuation tension profiles. On average, this tension is found to be lower at cell fronts than the mid-section. However, leaders with non-sticky followers are more prone to display higher tension at their front and have a negative correlation between cell speed and front-mid tension difference. We, thus, conclude that intracellular tension gradients are heterogeneous in cell sheets and substrate adhesivity of followers can control the coupling of the gradient to cell speed.</span></p>
Rapid increase in transferrin receptor recycling promotes adhesion during T cell activation
<p>This Dataset contains primary data used for the publication "Rapid increase in transferrin receptor recycling promotes adhesion during T cell activation" accepted for publication in BMC Biology on 15. July 2022</p> <p><strong>Abstract:</strong></p> <p>Background<br> T cell activation leads to increased expression of the receptor for the iron transporter transferrin (TfR) to provide iron required for the cell differentiation and clonal expansion that takes place during the days after encounter with a cognate antigen. However, T cells mobilise TfR to their surface within minutes after activation, although the reason and mechanism driving this process remain unclear.</p> <p>Results<br> Here we show that T cells transiently increase endocytic uptake and recycling of TfR upon activation, thereby boosting their capacity to import iron. We demonstrate that increased TfR recycling is powered by a fast endocytic sorting pathway relying on the membrane proteins flotillins, Rab5 and Rab11a-positive endosomes. Our data further reveal that iron import is required for a non-canonical signalling pathway involving the kinases Zap70 and PAK, which controls adhesion of the integrin LFA-1 and eventually leads to conjugation with antigen-presenting cells.</p> <p>Conclusions<br> Altogether, our data suggest that T cells boost their iron importing capacity immediately upon activation to promote adhesion to antigen-presenting cells.</p> <p> </p> <p>Data are organised in compressed (.zip) folders entitled as the corresponding Figures in the publication.</p> <p>Programs we recommend to view the files are:<br> .fcs files: FlowJo software v10 (Tree Star, Ashland, OR, USA)<br> .lsm and .czi files: ZEN 2012 SP1 and higher (Carl Zeiss, Jena, Germany)<br> .lif files: LAS X v3 (Leica Microsystems, Wetzlar, Germany)<br> .pzfx files: Prism v7 software (GraphPad, San Diego, CA, USA)</p>
Study of Propranolol as Anti-Adhesive Therapy in Sickle Cell Disease (SCD)
ClinicalTrials.gov study NCT01077921. IPD Sharing: Not stated. Countries: 1. Publications: 5.
The cell adhesion molecule Sdk1 shapes assembly of a retinal circuit that detects localized edges
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Data from: ESCRT-III-dependent adhesive and mechanical changes are triggered by a mechanism detecting alteration of Septate Junction integrity in Drosophila epithelial cells
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A multiscale theory for spreading and migration of adhesion-reinforced mesenchymal cells
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Effect of heterogeneous substrate adhesivity of follower cells on speed and tension profile of leader cells in primary keratocyte collective cell migration
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Center or Periphery? Modeling the Effects of Focal Adhesion Placement during Cell Spreading
<p>All data associate with paper Center or <em>Periphery? Modeling the Effects of Focal Adhesion Placement during Cell Spreading</em> by Magdalena Stolarska and Aravind Rammohan</p>
Supplementary videos: CD56/NCAM mediates cell migration of human NK cells by promoting integrin-mediated adhesion turnover [preprint]
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Correlating single-molecule rupture mechanics with cell population adhesion by yeast display
<p>Data underlying the figures in the publication “Correlating single-molecule rupture mechanics with cell population adhesion by yeast display”, published in <em>Biophysical Reports, </em><em><strong>2022</strong></em><em>, Volume 2, Issue 1, 100035, ISSN 2667-0747.</em></p> <p><em><a href="https://doi.org/10.1016/j.bpr.2021.100035">https://doi.org/10.1016/j.bpr.2021.100035</a></em></p> <p>Table of contents:</p> <p><strong>1. Fig2_SMFS.xlsx</strong>: Contour Length vs probability density values for <em>Figure 2D</em>. Rupture Force and Loading rate values for all SMFS curves analysed for <em>Figure 2E</em> and <em>2F</em>.</p> <p><strong>2. Fig3_SDA.xlsx</strong>: Shear Stress <em>vs</em> Cell Density values of all replicates and speeds for F<em>igures 3D</em> and <em>3E</em>.</p> <p><strong>3. FigS1_SPR curves.xlsx</strong>: SPR curves reported in Supplementary <em>Figure 1</em>.</p> <p><strong>4. FigS2_one step FLN.xlsx</strong>: Force <em>vs</em> Extension trace and Contour Length Histogram values for one step FLN unfolding shown in <em>Supplementary Figure 2</em>.</p> <p><strong>5. FigS3_SMFS_internal control.xlsx</strong>: Rupture Force and Loading rate values for N-S25H reported in <em>Supplementary Figure 3</em>.</p> <p><strong>6. FigS5_SDA_internal control.xlsx</strong>: Shear Stress <em>vs</em> Cell Density values of N-WT shown in <em>Supplementary figure 5B</em>.</p> <p><strong>7. FigS6_SDA_induction timepoints.xlsx</strong>: Shear Stress <em>vs</em> Cell Density values and median of expression detected by flow cytometry reported in <em>Supplementary Figure 6</em>.</p>
Wound Healing Assay Dataset (WHAD) and Cell Adhesion and Motility Assay Dataset (CAMAD)
<p>Please refer to the repository:<br>https://github.com/leonardo-iheme/whad_camad_datasets/tree/master</p>
Hexanematic crossover in epithelial monolayers depends on cell adhesion and cell density.
<p>Raw data files concerning the publication,</p> <p><strong>Hexanematic crossover in epithelial monolayers depends on cell adhesion and cell density</strong><br>Julia Eckert, Benoit Ladoux, Rene-Marc Mege, Luca Giomi and Thomas Schmidt<br>Nature Communications (2023) <strong>14</strong>:5762.<br>doi: <span>https://doi.org/10.1038/s41467-023-41449-6</span><br><br><strong>Abstract:</strong></p> <p>Changes in tissue geometry during developmental processes are associated with collective migration of cells. Recent experimental and numerical results suggest that these changes could leverage on the coexistence of nematic and hexatic orientational order at different length scales. How this multiscale organization is affected by the material properties of the cells and their substrate is presently unknown. In this study, we address these questions in monolayers of Madin-Darby canine kidney cells having various cell densities and molecular repertoires. At small length scales, confluent monolayers are characterized by a prominent hexatic order, independent of the presence of E-cadherin, monolayer density, and underlying substrate stiffness. However, all three properties affect the meso-scale tissue organization. The length scale at which hexatic order transits to nematic order, the ”hexanematic” crossover scale, strongly depends on cell-cell adhesions and correlates with monolayer density. Our study demonstrates how epithelial organization is affected by mechanical properties, and provides a robust description of tissue organization during developmental processes.</p> <p> </p> <p><strong>Data description:</strong></p> <p>WT.zip - zipped raw image data and extracted vertices of experiments on wild-type cells<br>KO.zip - zipped raw image data and extracted vertices of experiments on eCad KO-cells<br>FigureData.zip - zipped data referring to each of the figures in the paper</p> <p> </p> <p><strong>Software:</strong></p> <p>The software to analyze the data presented here is found on GitHub, [https://github.com/hexanematic/orientation tracker]</p>
Propanolol and Red Cell Adhesion Non-asthmatic Children Sickle Cell Disease
ClinicalTrials.gov study NCT02012777. IPD Sharing: YES. Countries: 1. Publications: 8.
Analysis of Lymphocyte Cell Surface Adhesion Marker Expression in Natalizumab Population With Active Control
ClinicalTrials.gov study NCT01626248. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Blood Cell Adhesion to Arterial Filters During Cardiac Surgery
ClinicalTrials.gov study NCT03882593. IPD Sharing: Not stated. Countries: 1. Publications: 3.
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Allen Brain Atlas
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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
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