Littérature scientifique sur le sujet « Lysosomes »

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Articles de revues sur le sujet "Lysosomes"

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Nakae, Isei, Tomoko Fujino, Tetsuo Kobayashi, et al. "The Arf-like GTPase Arl8 Mediates Delivery of Endocytosed Macromolecules to Lysosomes inCaenorhabditis elegans." Molecular Biology of the Cell 21, no. 14 (2010): 2434–42. http://dx.doi.org/10.1091/mbc.e09-12-1010.

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Late endocytic organelles including lysosomes are highly dynamic acidic organelles. Late endosomes and lysosomes directly fuse for content mixing to form hybrid organelles, from which lysosomes are reformed. It is not fully understood how these processes are regulated and maintained. Here we show that the Caenorhabditis elegans ARL-8 GTPase is localized primarily to lysosomes and involved in late endosome-lysosome fusion in the macrophage-like coelomocytes. Loss of arl-8 results in an increase in the number of late endosomal/lysosomal compartments, which are smaller than wild type. In arl-8 mu
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Trivedi, Purvi C., Jordan J. Bartlett, and Thomas Pulinilkunnil. "Lysosomal Biology and Function: Modern View of Cellular Debris Bin." Cells 9, no. 5 (2020): 1131. http://dx.doi.org/10.3390/cells9051131.

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Lysosomes are the main proteolytic compartments of mammalian cells comprising of a battery of hydrolases. Lysosomes dispose and recycle extracellular or intracellular macromolecules by fusing with endosomes or autophagosomes through specific waste clearance processes such as chaperone-mediated autophagy or microautophagy. The proteolytic end product is transported out of lysosomes via transporters or vesicular membrane trafficking. Recent studies have demonstrated lysosomes as a signaling node which sense, adapt and respond to changes in substrate metabolism to maintain cellular function. Lyso
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Amick, Joseph, Arun Kumar Tharkeshwar, Catherine Amaya,, and Shawn M. Ferguson. "WDR41 supports lysosomal response to changes in amino acid availability." Molecular Biology of the Cell 29, no. 18 (2018): 2213–27. http://dx.doi.org/10.1091/mbc.e17-12-0703.

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C9orf72 mutations are a major cause of amyotrophic lateral sclerosis and frontotemporal dementia. The C9orf72 protein undergoes regulated recruitment to lysosomes and has been broadly implicated in control of lysosome homeostasis. However, although evidence strongly supports an important function for C9orf72 at lysosomes, little is known about the lysosome recruitment mechanism. In this study, we identify an essential role for WDR41, a prominent C9orf72 interacting protein, in C9orf72 lysosome recruitment. Analysis of human WDR41 knockout cells revealed that WDR41 is required for localization
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Bonet-Ponce, Luis, Alexandra Beilina, Chad D. Williamson, et al. "LRRK2 mediates tubulation and vesicle sorting from lysosomes." Science Advances 6, no. 46 (2020): eabb2454. http://dx.doi.org/10.1126/sciadv.abb2454.

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Genetic variation around the LRRK2 gene affects risk of both familial and sporadic Parkinson’s disease (PD). However, the biological functions of LRRK2 remain incompletely understood. Here, we report that LRRK2 is recruited to lysosomes after exposure of cells to the lysosome membrane–rupturing agent LLOME. Using an unbiased proteomic screen, we identified the motor adaptor protein JIP4 as an LRRK2 partner at the lysosomal membrane. LRRK2 can recruit JIP4 to lysosomes in a kinase-dependent manner via the phosphorylation of RAB35 and RAB10. Using super-resolution live-cell imaging microscopy an
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Bakker, A. C., P. Webster, W. A. Jacob, and N. W. Andrews. "Homotypic fusion between aggregated lysosomes triggered by elevated [Ca2+]i in fibroblasts." Journal of Cell Science 110, no. 18 (1997): 2227–38. http://dx.doi.org/10.1242/jcs.110.18.2227.

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Previous studies demonstrated that microinjection of antibodies to the cytoplasmic domain of the lysosomal glycoprotein lgp120 induces aggregation of lysosomes in NRK cells. Here we show that the antibody-clustered vesicles do not co-localize with MPR and ss-COP-containing organelles, confirming their lysosomal nature. Observations by transmission and high voltage electron microscopy indicated that, although tightly apposed to each other, aggregated lysosomes remained as separate vesicles, with an average diameter of 0.3-0.4 micron. However, when cells microinjected with antibody were exposed
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Xu, Miao, Ke Liu, Manju Swaroop, et al. "A Phenotypic Compound Screening Assay for Lysosomal Storage Diseases." Journal of Biomolecular Screening 19, no. 1 (2013): 168–75. http://dx.doi.org/10.1177/1087057113501197.

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The lysosome is a vital cellular organelle that primarily functions as a recycling center for breaking down unwanted macromolecules through a series of hydrolases. Functional deficiencies in lysosomal proteins due to genetic mutations have been found in more than 50 lysosomal storage diseases that exhibit characteristic lipid/macromolecule accumulation and enlarged lysosomes. Recently, the lysosome has emerged as a new therapeutic target for drug development for the treatment of lysosomal storage diseases. However, a suitable assay for compound screening against the diseased lysosomes is curre
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Cuervo, A. M., E. Knecht, S. R. Terlecky, and J. F. Dice. "Activation of a selective pathway of lysosomal proteolysis in rat liver by prolonged starvation." American Journal of Physiology-Cell Physiology 269, no. 5 (1995): C1200—C1208. http://dx.doi.org/10.1152/ajpcell.1995.269.5.c1200.

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Lysosomal uptake and degradation of polypeptides such as glyceraldehyde-3-phosphate dehydrogenase (GAPDH), ribonuclease A (RNase A), and RNase S-peptide (residues 1-20 of RNase A) are progressively activated in rat liver by starvation before isolation of lysosomes. This pathway of proteolysis is selective, since it is stimulated by the heat shock cognate protein of 73 kDa (HSC73) and ATP-MgCl2, and lysosomal uptake of RNase A could be competed by GAPDH but not by ovalbumin. A portion of intracellular HSC73 is associated with certain lysosomes, and the amount of lysosomal HSC73 increases by 5-
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Liu, Ji, Wennan Lu, Sonia Guha, et al. "Cystic fibrosis transmembrane conductance regulator contributes to reacidification of alkalinized lysosomes in RPE cells." American Journal of Physiology-Cell Physiology 303, no. 2 (2012): C160—C169. http://dx.doi.org/10.1152/ajpcell.00278.2011.

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The role of the cystic fibrosis transmembrane conductance regulator (CFTR) in lysosomal acidification has been difficult to determine. We demonstrate here that CFTR contributes more to the reacidification of lysosomes from an elevated pH than to baseline pH maintenance. Lysosomal alkalinization is increasingly recognized as a factor in diseases of accumulation, and we previously showed that cAMP reacidified alkalinized lysosomes in retinal pigmented epithelial (RPE) cells. As the influx of anions to electrically balance proton accumulation may enhance lysosomal acidification, the contribution
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Alquier, C., P. Guenin, Y. Munari-Silem, C. Audebet, and B. Rousset. "Isolation of pig thyroid lysosomes. Biochemical and morphological characterization." Biochemical Journal 232, no. 2 (1985): 529–37. http://dx.doi.org/10.1042/bj2320529.

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Open thyroid follicles were prepared by mechanical disruption of pig thyroid fragments through a metal sieve. This procedure allowed preparation of thyroid-cell material depleted of colloid thyroglobulin. Open thyroid follicles were used to prepared a crude particulate fraction, which contained lysosomes, mitochondria and endoplasmic reticulum. These organelles were subfractionated by isopycnic centrifugation on iso-osmotic Percoll gradients. A lysosomal peak was identified by its content of acid hydrolases: acid phosphatase, cathepsin D, β-galactosidase and β-glucuronidase. The lysosomal peak
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Zeng, Wenping, Canjun Li, Ruikun Wu, et al. "Optogenetic manipulation of lysosomal physiology and autophagy-dependent clearance of amyloid beta." PLOS Biology 22, no. 4 (2024): e3002591. http://dx.doi.org/10.1371/journal.pbio.3002591.

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Lysosomes are degradation centers of cells and intracellular hubs of signal transduction, nutrient sensing, and autophagy regulation. Dysfunction of lysosomes contributes to a variety of diseases, such as lysosomal storage diseases (LSDs) and neurodegeneration, but the mechanisms are not well understood. Altering lysosomal activity and examining its impact on the occurrence and development of disease is an important strategy for studying lysosome-related diseases. However, methods to dynamically regulate lysosomal function in living cells or animals are still lacking. Here, we constructed lyso
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Thèses sur le sujet "Lysosomes"

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Ebrahim, Roshan. "Biogenesis of lysosomes in macrophages : intracellular pathway of lysosomal membrane protein to lysosomes." Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/3126.

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Salgues, Frédéric. "Ciblage des lysosomes pour la thérapie enzymatique substitutive ou pour la thérapie photodynamique." Thesis, Montpellier 2, 2011. http://www.theses.fr/2011MON20148.

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Le récepteur du mannose-6-phosphate cation indépendant (RM6P-CI) permet l'endocytose puis le transfert de molécules porteuses du marqueur M6P vers les lysosomes. Pour améliorer à la fois l'affinité pour le RM6P-CI et la stabilité du résidu M6P, nous avons procédé à la synthèse d'analogues isostères stables et fonctionnalisés en position anomère pour permettre un couplage efficace à des molécules d'intérêt thérapeutique. Tout d'abord un couplage à des enzymes recombinantes humaines a été réalisé. Le remodelage de la partie oligosaccharidique de l'enzyme lysosomale GAA, dont la déficience est re
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Deng, Yuping. "Studies of intraorganelle dynamics : the lysosome, the pre-lysosomal compartment, and the golgi apparatus /." Diss., This resource online, 1991. http://scholar.lib.vt.edu/theses/available/etd-07282008-134815/.

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Boutry, Maxime. "Dysfonctions des lysosomes et neurodégénérescence : l'exemple de la paraplégie spastique de type SPG11." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066295/document.

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Les lysosomes sont importants pour la survie et la fonction des cellules du système nerveux central et en particulier des neurones. Le mécanisme de la reformation des lysosomes est crucial pour maintenir une quantité adéquate de lysosomes fonctionnels dans les cellules. La spatacsine, qui joue un rôle dans le ce mécanisme est impliquée dans la paraplégie spastique de type SPG11 ; une maladie caractérisée par des troubles moteurs et cognitifs sévères. L’utilisation de modèles cellulaires de cette pathologie permet d’étudier les mécanismes physiopathologiques à l’origine d’altérations de la refo
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Moule, Christie Joy. "The synthesis and kinetic studies of substrate analogues for N-acetylgalactosamine-4-sulfatase." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phm926.pdf.

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Piccolo, Enzo. "Rôle de la protéine HMGB1 dérivée des macrophages au cours d'une réaction inflammatoire." Thesis, Toulouse 3, 2021. http://www.theses.fr/2021TOU30035.

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La réaction inflammatoire est la première étape nécessaire pour restaurer l'homéostasie tissulaire lésée. Elle implique au cours de ses différentes étapes, le système immunitaire, notamment les macrophages qui présentent alors divers remaniements inflammatoires et métaboliques. Les macrophages sont capables de modifier et d'adapter leur métabolisme cellulaire afin de satisfaire leurs besoins énergétiques et réaliser de façon efficace la réaction inflammatoire en fonction des signaux du milieu environnant. Ces adaptations métaboliques influencent la physiologie des mitochondries et les oxydatio
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Kågedal, Katarina. "Cathepsin D released from lysosomes mediates apoptosis /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med771s.pdf.

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Selmi, Samia. "Études biochimiques et fonctionnelles des lysosomes thyroïdiens." Lyon 1, 1989. http://www.theses.fr/1989LYO1T049.

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Jakhria, Toral Chandulal. "Amyloid fibrils are nanoparticles that target lysosomes." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/7628/.

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The amyloidoses are a group of debilitating disorders which include neurodegenerative diseases such as Alzheimer’s disease and systemic diseases such as dialysis-related amyloidosis (DRA). Amyloidoses are associated with the aggregation of proteins into amyloid fibrils with a highly organised cross-β structure. Amyloid fibrils are formed by a variety of proteins and peptides despite differences in sequence and native structure. Amyloid formation occurs by a nucleated growth mechanism and proceeds via oligomeric intermediates into mature fibrils. Despite intense research, the molecular mechanis
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Atakpa, Peace. "Ca2+ signalling between the endoplasmic reticulum and lysosomes." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288002.

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Ca2+ is a universal and versatile intracellular messenger, regulating a vast array of biological processes due to variations in the frequency, amplitude, spatial and temporal dynamics of Ca2+ signals. Increases in cytosolic free Ca2+ concentration ([Ca2+]c) are due to influx from either an infinite extracellular Ca2+ pool or from the more limited intracellular Ca2+ stores. Stimulation of the endogenous muscarinic (M3) receptors of human embryonic kidney (HEK) cells with carbachol results in the activation of phospholipase C (PLC) and formation of inositol 1,4,5-trisphosphate (IP3), activation
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Livres sur le sujet "Lysosomes"

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Holtzman, Eric. Lysosomes. Plenum Press, 1989.

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Öllinger, Karin, and Hanna Appelqvist, eds. Lysosomes. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6934-0.

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Holtzman, Eric. Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4.

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Holtzman, Eric. Lysosomes. Plenum Press, 1989.

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Mehta, Atul B., and Bryan Winchester. Lysosomal storage disorders: A practical guide. Wiley-Blackwell, 2013.

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Maxfield, Frederick R., James M. Willard, and Shuyan Lu, eds. Lysosomes: Biology, Diseases, and Therapeutics. John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118978320.

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G, Thoene Jess, ed. Pathophysiology of lysosomal transport. CRC Press, 1992.

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Reunov, A. V. Liticheskai︠a︡ funkt︠s︡ii︠a︡ kletki. Nauka, 2008.

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Lin, Yuxi. Role of Lysosomes in Nonshivering Thermogenesis. [publisher not identified], 2016.

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H, Glaumann, and Ballard F. J, eds. Lysosomes: Their role in protein breakdown. Academic Press, 1987.

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Chapitres de livres sur le sujet "Lysosomes"

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Kuma, Akiko, and Tamotsu Yoshimori. "Pathways to Repair or Remove Lysosomes Damaged by Extracellular Fine Particles." In Extracellular Fine Particles. Springer Nature Singapore, 2025. https://doi.org/10.1007/978-981-97-7067-0_13.

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Abstract Exogenous and endogenous fine particles such as environmental materials (e.g., silica, asbestos, alum), toxic protein aggregates (e.g., α-synuclein, amyloid-β), and endogenous crystals (e.g., cholesterol crystals, uric acid crystals) are internalized into the cell by the endocytic pathway or phagocytosis. Because lysosomes are the terminal compartments of these pathways, lysosomes are known to be damaged by exocytosed extracellular fine particles. Lysosomal membrane damage allows the leakage of the lysosomal contents such as cathepsins, H+, Ca2+, and iron into the cytosol, which is ha
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Holtzman, Eric. "Historical Fragments; Methods; Some Terminology." In Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_1.

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Holtzman, Eric. "Endocytosis and Heterophagy." In Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_2.

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Holtzman, Eric. "Acidification; Membrane Properties; Permeability and Transport." In Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_3.

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Holtzman, Eric. "Uses and Abuses of Endocytotic and Heterophagic Pathways." In Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_4.

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Holtzman, Eric. "Autophagy and Related Phenomena." In Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_5.

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Holtzman, Eric. "Extensive Release. Excessive Storage." In Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_6.

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Holtzman, Eric. "Genesis." In Lysosomes. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_7.

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Valk, Jacob, and Marjo S. van der Knaap. "Lysosomes and Lysosomal Disorders." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-02568-0_6.

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Wevers, R. A., and V. Gieselmann. "Lysosomes and Lysosomal Disorders." In Magnetic Resonance of Myelination and Myelin Disorders. Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27660-2_5.

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Actes de conférences sur le sujet "Lysosomes"

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Giugliano, Giusy, Michela Schiavo, Daniele Pirone, et al. "Investigation on lysosomal accumulation by a quantitative analysis of 2D phase-maps in digital holography microscopy." In Digital Holography and Three-Dimensional Imaging. Optica Publishing Group, 2024. http://dx.doi.org/10.1364/dh.2024.th2a.6.

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Quantitative Phase Imaging through Digital Holography (QPI-DH) represents a quantitative and label-free method to detect lysosomal dysfunction in cells. Testing in the cellular model of Mucopolysaccharidosis type III-A, a lysosomal storage disease, demonstrate its potential.
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Zhu, X. "Relationship Between Autophagy-Lysosomes Pathway and Ventilator-Induced Diaphragmatic Dysfunction." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2622.

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Perera, Rushika M. "Abstract I22: New players and unique features of cancer lysosomes." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-i22.

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Bakhit, C., D. Lewis, R. Billings, and B. Malfroy. "CELLULAR CATABOLISM OF RECOMBINANT TISSUE-TYPE PLASMINOGEN ACTIVATOR: IDENTIFICATION AND CHARACTERIZATION OF A NOVEL HIGH AFFINITY UPTAKE SYSTEM ON RAT HEPATOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644400.

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The uptake, internalization and intracellular degradation of 125I-labeled rt-PA (125I-rt-PA) by isolated rat hepatocytes was investigated. Incubation at 37°C resulted in internalization of 125I-rt-PA, followed by the appearance of labeled trichloroacetic acid-soluble (TCA) material in the inclubation media due to degradation of rt-PA. Degradation of rt-PA was inhibited by the presence of NH4Cl (10mM) or chloroquine (ImM) (lysosoma tropic agents) in the incubation media. This suggests that rt-PA degradation occurs intracellularly, perhaps within the lysosomes. 125I-rt-PA was taken up by rat hep
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Hung, Hsin-I., Geraldine Quiogue, John J. Lemasters, and Anna-Liisa Nieminen. "Signaling from lysosomes to mitochondria sensitizes cancer cells to photodynamic treatment." In SPIE BiOS, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2011. http://dx.doi.org/10.1117/12.878306.

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Quiogue, Geraldine, Shalini Saggu, Hsin-I. Hung, et al. "Signaling from lysosomes enhances mitochondria-mediated photodynamic therapy in cancer cells." In 12th World Congress of the International Photodynamic Association, edited by David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.823752.

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Joncour, Vadim Le, Pauliina Filppu, Minna Holopainen, et al. "Abstract LB-055: Novel therapeutic option targeting the tumor cell lysosomes." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-lb-055.

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Tang, Hao-yang, Meng Qian, Cong Song, and Yi-chao Zhang. "Lysosomes Computational Labeling Method Based on Feature Map Slice of Deeplabv3+." In 2019 IEEE Symposium Series on Computational Intelligence (SSCI). IEEE, 2019. http://dx.doi.org/10.1109/ssci44817.2019.9002802.

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Nieminen, Anna-Liisa, Kashif Azizuddin, Ping Zhang, et al. "Contribution of mitochondria and lysosomes to photodynamic therapy-induced death in cancer cells." In Biomedical Optics (BiOS) 2008, edited by David Kessel. SPIE, 2008. http://dx.doi.org/10.1117/12.767356.

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Metelitsina, Irina P., and N. F. Leus. "Action of low-energy monochromatic coherent light on the stability of retinal lysosomes." In Photonics West '95, edited by Steven L. Jacques. SPIE, 1995. http://dx.doi.org/10.1117/12.209925.

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Rapports d'organisations sur le sujet "Lysosomes"

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Levenson, Victor V. Lysosome-mediated Cell Death and Autophagy-Dependent Multidrug Resistance in Breast Cancer. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada495800.

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Shiio, Yuzuru. Targeting Androgen Receptor by Lysosomal Degradation in Prostate Cancer. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada612607.

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Shiio, Yuzuru. Targeting Androgen Receptor by Lysosomal Degradation in Prostate Cancer. Defense Technical Information Center, 2015. http://dx.doi.org/10.21236/ada621824.

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Palmer, Guy, Varda Shkap, Wendy Brown, and Thea Molad. Control of bovine anaplasmosis: cytokine enhancement of vaccine efficacy. United States Department of Agriculture, 2007. http://dx.doi.org/10.32747/2007.7695879.bard.

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Anaplasmosis an arthropod-born disease of cattle caused by the rickettsia Anaplasma marginale and is an impediment to efficient production of healthy livestock in both Israel and the United States. Currently the only effective vaccines are derived from the blood of infected cattle. The risk of widespread transmission of both known and newly emergent pathogens has prevented licensure of live blood-based vaccines in the U.S. and is a major concern for their continued use in Israel. Consequently development of a safe, effective vaccine is a high priority. In this collaborative project we focused
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