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Relevant bibliographies by topics / EVs trafficking

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Journal articles

Academic literature on the topic 'EVs trafficking'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "EVs trafficking"

1

Maire, Cecile, Amanda Salviano-Silva, Katharina Kolbe, Manfred Westphal, Katrin Lamszus, and Franz Ricklefs. "TMIC-64. EXTRACELLULAR VESICLE TRAFFICKING IN GBM." Neuro-Oncology 24, Supplement_7 (2022): vii285—vii286. http://dx.doi.org/10.1093/neuonc/noac209.1108.

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Abstract Extracellular vesicles (EVs) are secreted by all cell types, including tumor cells, and are found in increased numbers in the plasma of GBM patients. EVs may contain high-value genetic material that can be useful for tracking tumor development, as well as membrane proteins that affect other cells. This prompted us to investigate how tumor EVs might influence immune cells in glioma, and in primary and secondary lymphoid organs as well as in the circulation. To this end we used a syngeneic GBM mouse model and tracked tumor EVs from the brain to the meninges, cervical lymph nodes, plasma

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Kumar, Prashant, Fahad Zadjali, Ying Yao, et al. "Single Gene Mutations in Pkd1 or Tsc2 Alter Extracellular Vesicle Production and Trafficking." Biology 11, no. 5 (2022): 709. http://dx.doi.org/10.3390/biology11050709.

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Patients with autosomal dominant polycystic kidney disease (ADPKD) and tuberous sclerosis complex (TSC) are born with normal or near-normal kidneys that later develop cysts and prematurely lose function. Both renal cystic diseases appear to be mediated, at least in part, by disease-promoting extracellular vesicles (EVs) that induce genetically intact cells to participate in the renal disease process. We used centrifugation and size exclusion chromatography to isolate the EVs for study. We characterized the EVs using tunable resistive pulse sensing, dynamic light scattering, transmission electr

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Santamaria, Sara, Maria Cristina Gagliani, Grazia Bellese, et al. "Imaging of Endocytic Trafficking and Extracellular Vesicles Released Under Neratinib Treatment in ERBB2+ Breast Cancer Cells." Journal of Histochemistry & Cytochemistry 69, no. 7 (2021): 461–73. http://dx.doi.org/10.1369/00221554211026297.

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Breast cancers (BCa) with ERBB2 amplification show rapid tumor growth, increased disease progression, and lower survival rate. Deregulated intracellular trafficking and extracellular vesicle (EVs) release are mechanisms that support cancer progression and resistance to treatments. Neratinib (NE) is a Food and Drug Administration–approved pan-ERBB inhibitor employed for the treatment of ERBB2+ BCa that blocks signaling and causes survival inhibition. However, the effects of NE on ERBB2 internalization, its trafficking to multivesicular bodies (MVBs), and the release of EVs that originate from t

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Baxter, Amy A. "Stoking the Fire: How Dying Cells Propagate Inflammatory Signalling through Extracellular Vesicle Trafficking." International Journal of Molecular Sciences 21, no. 19 (2020): 7256. http://dx.doi.org/10.3390/ijms21197256.

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Communication between dying cells and their environment is a critical process that promotes tissue homeostasis during normal cellular turnover, whilst during disease settings, it can contribute to inflammation through the release of intracellular factors. Extracellular vesicles (EVs) are a heterogeneous class of membrane-bound cell-derived structures that can engage in intercellular communication via the trafficking of bioactive molecules between cells and tissues. In addition to the well-described functions of EVs derived from living cells, the ability of dying cells to release EVs capable of

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Roberts-Dalton, H. D., A. Cocks, J. M. Falcon-Perez, et al. "Fluorescence labelling of extracellular vesicles using a novel thiol-based strategy for quantitative analysis of cellular delivery and intracellular traffic." Nanoscale 9, no. 36 (2017): 13693–706. http://dx.doi.org/10.1039/c7nr04128d.

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6

Ortega, Miguel A., Oscar Fraile-Martinez, Cielo Garcia-Montero, et al. "An Updated View of the Importance of Vesicular Trafficking and Transport and Their Role in Immune-Mediated Diseases: Potential Therapeutic Interventions." Membranes 12, no. 6 (2022): 552. http://dx.doi.org/10.3390/membranes12060552.

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Cellular trafficking is the set of processes of distributing different macromolecules by the cell. This process is highly regulated in cells, involving a system of organelles (endomembranous system), among which are a great variety of vesicles that can be secreted from the cell, giving rise to different types of extracellular vesicles (EVs) that can be captured by other cells to modulate their function. The cells of the immune system are especially sensitive to this cellular traffic, producing and releasing different classes of EVs, especially in disease states. There is growing interest in th

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7

Cruz Camacho, Abel, Daniel Alfandari, Ewa Kozela, and Neta Regev-Rudzki. "Biogenesis of extracellular vesicles in protozoan parasites: The ESCRT complex in the trafficking fast lane?" PLOS Pathogens 19, no. 2 (2023): e1011140. http://dx.doi.org/10.1371/journal.ppat.1011140.

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Extracellular vesicles (EVs) provide a central mechanism of cell–cell communication. While EVs are found in most organisms, their pathogenesis-promoting roles in parasites are of particular interest given the potential for medical insight and consequential therapeutic intervention. Yet, a key feature of EVs in human parasitic protozoa remains elusive: their mechanisms of biogenesis. Here, we survey the current knowledge on the biogenesis pathways of EVs secreted by the four main clades of human parasitic protozoa: apicomplexans, trypanosomatids, flagellates, and amoebae. In particular, we shin

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Zhang, Pan, Su Bin Lim, Kuan Jiang, Ti Weng Chew, Boon Chuan Low, and Chwee Teck Lim. "Distinct mRNAs in Cancer Extracellular Vesicles Activate Angiogenesis and Alter Transcriptome of Vascular Endothelial Cells." Cancers 13, no. 9 (2021): 2009. http://dx.doi.org/10.3390/cancers13092009.

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Cancer-derived extracellular vesicles (EVs) have been demonstrated to be implicated in various processes of cancer development, with most of the EV-induced changes attributed to EV-proteins and EV-microRNAs. However, the knowledge about the abundance of cancer EV-mRNAs and their contribution to cancer development remain elusive. Here, we show that mRNAs prevail in cancer EVs as compared with normal EVs, and cancer EVs that carry abundant angiogenic mRNAs activate angiogenesis in human umbilical vein endothelial cells (HUVECs). Specifically, of a gene panel comprising 61 hypoxia-targeted oncoge

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Auger, Clément, Aude Brunel, Tiffany Darbas, et al. "Extracellular Vesicle Measurements with Nanoparticle Tracking Analysis: A Different Appreciation of Up and Down Secretion." International Journal of Molecular Sciences 23, no. 4 (2022): 2310. http://dx.doi.org/10.3390/ijms23042310.

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As is the case with most eucaryotic cells, cancer cells are able to secrete extracellular vesicles (EVs) as a communication means towards their environment and surrounding cells. EVs are represented by microvesicles and smaller vesicles called exosomes, which are known for their involvement in cancer aggressiveness. The release of such EVs requires the intervention of trafficking-associated proteins, mostly represented by the RAB-GTPases family. In particular, RAB27A is known for its role in addressing EVs-to-be secreted towards the the plasma membrane. In this study, shRNAs targeting RAB27A w

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Lipinski, Simone, and Katharina Tiemann. "Extracellular Vesicles and Their Role in the Spatial and Temporal Expansion of Tumor–Immune Interactions." International Journal of Molecular Sciences 22, no. 7 (2021): 3374. http://dx.doi.org/10.3390/ijms22073374.

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Extracellular vesicles (EVs) serve as trafficking vehicles and intercellular communication tools. Their cargo molecules directly reflect characteristics of their parental cell. This includes information on cell identity and specific cellular conditions, ranging from normal to pathological states. In cancer, the content of EVs derived from tumor cells is altered and can induce oncogenic reprogramming of target cells. As a result, tumor-derived EVs compromise antitumor immunity and promote cancer progression and spreading. However, this pro-oncogenic phenotype is constantly being challenged by E

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