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40 results for “Endocytosis”
The functions of cholera toxin subunit B as a modulator of silica nanoparticle endocytosis
<p>The gastrointestinal tract is the main target of orally ingested nanoparticles (NPs) and at 9 the same time exposed to noxious substances, such as bacterial components. We investigated the 10 interaction of 59 nm silica (SiO2) NPs with differentiated Caco-2 intestinal epithelial cells in the pres-11 ence of cholera toxin subunit B (CTxB) and compared the effects to J774A.1 macrophages. CTxB can 12 affect cellular functions and modulate endocytosis via binding to the monosialoganglioside (GM1) 13 receptor, expressed on both cell lines. After stimulating macrophages with CTxB, we observed no-14 table changes in the membrane structure but not in Caco-2 cells and no secretion of the pro-inflam-15 matory cytokine TNF-α was detected. Cells were then exposed to 59 nm SiO2 NPs and CtxB sequen-16 tially and simultaneously, resulting in a high NPs uptake in J774A.1 cells but no uptake in Caco-2 17 cells was detected. Flow cytometry analysis revealed that exposure of J774A.1 cells to CTxB resulted 18 in a significant reduction in the uptake of SiO2 NPs. In contrast, the uptake of NPs by highly selective 19 Caco-2 cells remained unaffected following CTxB exposure. Based on colocalization studies, CTxB 20 and NPs might enter cells via shared endocytic pathways, followed by their sorting into different 21 intracellular compartments. Our findings provide new insights into the CTxB function to modulate 22 SiO2 NPs uptake in phagocytic but not in differentiated intestine cells.</p>
Domain-specific model selection for structural identification of the Rab5-Rab7 dynamics in endocytosis - Additional Files
<p>Additional files from the manuscript titled "Domain-specific model selection for structural identification of the Rab5-Rab7 dynamics in endocytosis" published in BMC Systems Biology:</p> <ul> <li>Data containing delimited time points and measurements used for fitting the different model structures</li> <li>Supplementary material containing additional figures and tables</li> <li>Archive containing the complete library, the incomplete model and the task used for modeling the Rab5-Rab7 switch</li> </ul> <p> </p>
Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis
<p><strong>Abstract</strong></p> <p>Vascular endothelial (VE)-cadherin in endothelial adherens junctions is an essential component of the vascular barrier, critical for tissue homeostasis and implicated in diseases such as cancer and retinopathies. Inhibitors of Src cytoplasmic tyrosine kinase have been applied to suppress VE-cadherin tyrosine phosphorylation and prevent excessive leakage, edema and high interstitial pressure. Here we show that the Src-related Yes tyrosine kinase, rather than Src, is localized at endothelial cell (EC) junctions where it becomes activated in a flow-dependent manner. EC-specific <em>Yes1</em> deletion suppresses VE-cadherin phosphorylation and arrests VE-cadherin at EC junctions. This is accompanied by loss of EC collective migration and exaggerated agonist-induced macromolecular leakage. Overexpression of <em>Yes1</em> causes ectopic VE-cadherin phosphorylation, while vascular leakage is unaffected. In contrast, in EC-specific Src-deficiency, VE-cadherin internalization is maintained, and leakage is suppressed. In conclusion, Yes-mediated phosphorylation regulates constitutive VE-cadherin turnover, thereby maintaining endothelial junction plasticity and vascular integrity.</p> <p><strong>Method for retinal EC distribution analysis</strong></p> <p>Chimeric recombination was induced in iSuRe-Cre+ mice at P3 by i.p. injection of tamoxifen (100 µg/mouse, Sigma). Retinas were taken at P7 and P15, immunostained for CD31 and flat-mounted. Images were taken by z-stack tile scanning using a 10X objective on a confocal microscope (Leica SP8). Maximum intensity projection images of whole retinas were used for image segmentation, which was performed with ImageJ resources. The maximum projection of the MbTomato channel threshold was established to distinguish MbTomato+ cells from the background. Outliers with a radius between 0.2-1.0 µm were removed. The CD31 channel (after maximum projection) was used to define the outlines of veins and arteries; the optic nerve was used as a mask to define a referential system. For computational analysis, a bespoken Python-based workflow was employed, accessible on GitHub (https://github.com/wgiese/retina-vein-artery-cs). For every pixel in the image, three numbers were computed (using the mask as referential): (1) distance to the nearest vein (d<sub>v</sub>), (2) distance to the nearest artery (d<sub>a</sub>) and (3) radial distance to the optic nerve (r). From these measures, the relative distances by ϕ<sub>v-a</sub> = d<sub>v/</sub>(d<sub>v</sub> + d<sub>a</sub>) were obtained. The EC distribution was computed by performing the operation for all YFP-positive pixels, which were used as a proxy for EC distribution. A kernel density estimation was used to approximate the underlying EC distribution in the 2D coordinate system spanned by ϕ<sub>v-a</sub> and r. </p>
Cdc42 couples T cell receptor endocytosis to GRAF1-mediated tubular invaginations of the plasma membrane
<p>This Dataset contains primary data used for the publication "Cdc42 couples T cell receptor endocytosis to GRAF1-mediated tubular invaginations of the plasma membrane" published online on 04. November 2019<br> doi:10.3390/cells8111388</p> <p><strong>Abstract:</strong> T cell activation is immediately followed by internalization of the T cell receptor (TCR).<br> TCR endocytosis is required for T cell activation, but the mechanisms supporting removal of TCR<br> from the cell surface remain incompletely understood. Here we report that TCR endocytosis is<br> linked to the clathrin-independent carrier (CLIC) and GPI-enriched endocytic compartments<br> (GEEC) endocytic pathway. We show that unlike the canonical clathrin cargo transferrin or the<br> adaptor protein Lat, internalized TCR accumulates in tubules shaped by the small GTPase Cdc42<br> and the Bin/amphiphysin/Rvs (BAR) domain containing protein GRAF1 in T cells. Preventing<br> GRAF1-positive tubules to mature into endocytic vesicles by expressing a constitutively active<br> Cdc42 impairs the endocytosis of TCR, while having no consequence on the uptake of transferrin.<br> Together, our data reveal a link between TCR internalization and the CLIC/GEEC endocytic route<br> supported by Cdc42 and GRAF1.</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> .lif files: LAS X v3 (Leica Microsystems, Wetzlar, Germany)<br> .pzfx files: Prism v7 software (GraphPad, San Diego, CA, USA)</p> <p> </p> <p>In case this Dataset is updated, new version will be available with doi:10.5281/zenodo.3545842</p>
Data from: The clathrin adaptor complex AP-2 mediates endocytosis of BRASSINOSTEROID INSENSITIVE1 in Arabidopsis
Clathrin-mediated endocytosis (CME) regulates many aspects of plant development, including hormone signaling and responses to environmental stresses. Despite the importance of this process, the machinery that regulates CME in plants is largely unknown. In mammals, the heterotetrameric ADAPTOR PROTEIN COMPLEX-2 (AP-2) is required for the formation of clathrin-coated vesicles at the plasma membrane (PM). Although the existence of AP-2 has been predicted in Arabidopsis thaliana, the biochemistry and functionality of the complex is still uncharacterized. Here, we identified all the subunits of the Arabidopsis AP-2 by tandem affinity purification and found that one of the large AP-2 subunits, AP2A1, localized at the PM and interacted with clathrin. Furthermore, endocytosis of the leucine-rich repeat receptor kinase, BRASSINOSTEROID INSENSITIVE1 (BRI1), was shown to depend on AP-2. Knockdown of the two Arabidopsis AP2A genes or overexpression of a dominant-negative version of the medium AP-2 subunit, AP2M, impaired BRI1 endocytosis and enhanced the brassinosteroid signaling. Our data reveal that the CME machinery in Arabidopsis is evolutionarily conserved and that AP-2 functions in receptor-mediated endocytosis.
Data for: Intersectin1 promotes clathrin-mediated endocytosis by organizing and stabilizing endocytic protein interaction networks
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Research data supporting "Porous silicon nanoneedles modulate endocytosis to deliver biological payloads"
<p>Research data supporting of Gopal S. et al., 2019, Advanced Materials, DOI: 10.1002/adma.201806788</p>
Raw data for Jin et. al "Intersectin1 promotes clathrin-mediated endocytosis by organizing and stabilizing endocytic protein interaction networks"
<h2><strong><span>Intersectin1 promotes clathrin-mediated endocytosis by organizing and stabilizing endocytic protein interaction networks</span></strong></h2> <p><span> </span></p> <p><span>Meiyan Jin<sup>1,2*</sup>, Yuichiro Iwamoto<sup>1</sup>, Cyna Shirazinejad<sup>1</sup>, David G. Drubin<sup>1,3**</sup></span></p> <p><sup><span>1 </span></sup><span>Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA</span></p> <p><sup><span>2</span></sup><span> Current Address: Department of Biology, University of Florida, Gainesville, Fl 32611, USA</span></p> <p><sup><span>3</span></sup><span> Lead author</span></p> <p><sup><span>* </span></sup><span>Correspondence: meiyan.jin@ufl.edu</span></p> <p><sup><span>**</span></sup><span>Correspondence: </span><span>drubin@berkeley.edu</span></p>
Data from: The clathrin adaptor complex AP-2 mediates endocytosis of BRASSINOSTEROID INSENSITIVE1 in Arabidopsis
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Specific binding sites on Rhesus rotavirus capsid protein dictates the method of endocytosis inducing the murine model of biliary atresia
GEO Series GSE267721. Mus musculus. 6 samples. Type: Expression profiling by array.
MicroRNA analysis of the bovine alveolar macrophage response to Mycobacterium bovis infection suggests pathogen survival is enhanced by miRNA regulation of endocytosis and lysosome trafficking
GEO Series GSE58883. Bos taurus. 88 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Spns1 controls megalin dependent endocytosis via iron misregulation
GEO Series GSE268837. Mus musculus. 13 samples. Type: Expression profiling by high throughput sequencing.
Mucin-type O-glycosylation controls pluripotency in mouse embryonic stem cells via Wnt receptor endocytosis
GEO Series GSE152688. Mus musculus. 1 samples. Type: Expression profiling by high throughput sequencing.
MAD2-dependent insulin receptor endocytosis regulates metabolic homeostasis
GEO Series GSE240578. Mus musculus. 20 samples. Type: Expression profiling by high throughput sequencing.
The small iridoid compound genipin prevents alpha-synuclein aggregation and toxicity by affecting endocytosis, metabolism and lipid storage
GEO Series GSE226744. Saccharomyces cerevisiae. 12 samples. Type: Expression profiling by high throughput sequencing.
Nanoparticle stereochemistry-dependent endocytosis improves in vivo mRNA delivery
GEO Series GSE181333. Mus musculus. 3 samples. Type: Expression profiling by high throughput sequencing.
Canonical Wnt Induces Focal Adhesion and Integrin Beta-1 Endocytosis
GEO Series GSE193381. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing.
Synaptic vesicle endocytosis deficits underlie GBA-linked cognitive dysfunction in Parkinson’s disease and Dementia with Lewy bodies
GEO Series GSE283187. Mus musculus. 15 samples. Type: Expression profiling by high throughput sequencing.
Suppression of NCALD protects against spinal muscular atrophy by restoring impaired endocytosis
GEO Series GSE58316. Homo sapiens. 12 samples. Type: Expression profiling by array.
Involvement of endocytosis and alternative splicing in the formation of the pathological process in Parkinson's Disease
GEO Series GSE54536. Homo sapiens. 10 samples. Type: Expression profiling by array.
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