Relevant bibliographies by topics / Lysosomale Degradation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Lysosomale Degradation'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Lysosomale Degradation"

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Parkinson-Lawrence, Emma J., Tetyana Shandala, Mark Prodoehl, Revecca Plew, Glenn N. Borlace, and Doug A. Brooks. "Lysosomal Storage Disease: Revealing Lysosomal Function and Physiology." Physiology 25, no. 2 (2010): 102–15. http://dx.doi.org/10.1152/physiol.00041.2009.

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The discovery over five decades ago of the lysosome, as a degradative organelle and its dysfunction in lysosomal storage disorder patients, was both insightful and simple in concept. Here, we review some of the history and pathophysiology of lysosomal storage disorders to show how they have impacted on our knowledge of lysosomal biology. Although a significant amount of information has been accrued on the molecular genetics and biochemistry of lysosomal storage disorders, we still do not fully understand the mechanistic link between the storage material and disease pathogenesis. However, the a
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Lakatos, Lőrincz, Szabó, et al. "Sec20 is Required for Autophagic and Endocytic Degradation Independent of Golgi-ER Retrograde Transport." Cells 8, no. 8 (2019): 768. http://dx.doi.org/10.3390/cells8080768.

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Endocytosis and autophagy are evolutionarily conserved degradative processes in all eukaryotes. Both pathways converge to the lysosome where cargo is degraded. Improper lysosomal degradation is observed in many human pathologies, so its regulatory mechanisms are important to understand. Sec20/BNIP1 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 1) is a BH3 (Bcl-2 homology 3) domain-containing SNARE (soluble N-ethylmaleimide-sensitive factor-attachment protein receptors) protein that has been suggested to promote Golgi-ER retrograde transport, mitochondrial fission, apoptosis and mitop
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Zunke, Friederike. "The function of lysosomes and their role in Parkinson’s disease." Neuroforum 26, no. 1 (2020): 43–51. http://dx.doi.org/10.1515/nf-2019-0035.

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AbstractLysosomes are cellular organelles that are important for the degradation and recycling of various biomolecules. Specialized lysosomal membrane proteins, as well as soluble enzymes, are important for the efficient turn-over of lysosomal substrates. A deficiency in the degradative capacity of lysosomes leads to severe pathologies referred to as lysosomal storage disorders. There is increasing evidence for the importance of lysosomal function in neurodegenerative disorders, including Parkinson’s disease. One reason for this might be the vulnerability of neuronal cells. Since neurons do no
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Majumder, Priyanka, and Oishee Chakrabarti. "ESCRTs and associated proteins in lysosomal fusion with endosomes and autophagosomes." Biochemistry and Cell Biology 94, no. 5 (2016): 443–50. http://dx.doi.org/10.1139/bcb-2016-0099.

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Endolysosomal and autophagosomal degradation pathways are highly connected at various levels, sharing multiple molecular effectors that modulate them individually or simultaneously. These two lysosomal degradative pathways are primarily involved in the disposal of cargo internalized from the cell surface or long-lived proteins or aggregates and aged organelles present in the cytosol. Both of these pathways involve a number of carefully regulated vesicular fusion events that are dependent on ESCRT proteins. The ESCRT proteins especially ESCRT-I and III participate in the regulation of fusion ev
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Zhong, Xi Zoë, Yuanjie Zou, Xue Sun, et al. "Inhibition of Transient Receptor Potential Channel Mucolipin-1 (TRPML1) by Lysosomal Adenosine Involved in Severe Combined Immunodeficiency Diseases." Journal of Biological Chemistry 292, no. 8 (2017): 3445–55. http://dx.doi.org/10.1074/jbc.m116.743963.

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Impaired adenosine homeostasis has been associated with numerous human diseases. Lysosomes are referred to as the cellular recycling centers that generate adenosine by breaking down nucleic acids or ATP. Recent studies have suggested that lysosomal adenosine overload causes lysosome defects that phenocopy patients with mutations in transient receptor potential channel mucolipin-1 (TRPML1), a lysosomal Ca2+ channel, suggesting that lysosomal adenosine overload may impair TRPML1 and then lead to subsequent lysosomal dysfunction. In this study, we demonstrate that lysosomal adenosine is elevated
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Gullapalli, Anuradha, Breann L. Wolfe, Courtney T. Griffin, Terry Magnuson, and JoAnn Trejo. "An Essential Role for SNX1 in Lysosomal Sorting of Protease-activated Receptor-1: Evidence for Retromer-, Hrs-, and Tsg101-independent Functions of Sorting Nexins." Molecular Biology of the Cell 17, no. 3 (2006): 1228–38. http://dx.doi.org/10.1091/mbc.e05-09-0899.

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Sorting nexin 1 (SNX1) and SNX2 are the mammalian homologues of the yeast Vps5p retromer component that functions in endosome-to-Golgi trafficking. SNX1 is also implicated in endosome-to-lysosome sorting of cell surface receptors, although its requirement in this process remains to be determined. To assess SNX1 function in endocytic sorting of protease-activated receptor-1 (PAR1), we used siRNA to deplete HeLa cells of endogenous SNX1 protein. PAR1, a G-protein-coupled receptor, is proteolytically activated by thrombin, internalized, sorted predominantly to lysosomes, and efficiently degraded.
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Li, Guangbi, Jason Kidd, and Pin-Lan Li. "Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases." International Journal of Molecular Sciences 21, no. 5 (2020): 1559. http://dx.doi.org/10.3390/ijms21051559.

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Podocytes are visceral epithelial cells covering the outer surface of glomerular capillaries in the kidney. Blood is filtered through the slit diaphragm of podocytes to form urine. The functional and structural integrity of podocytes is essential for the normal function of the kidney. As a membrane-bound organelle, lysosomes are responsible for the degradation of molecules via hydrolytic enzymes. In addition to its degradative properties, recent studies have revealed that lysosomes may serve as a platform mediating cellular signaling in different types of cells. In the last decade, increasing
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Blumenreich, Shani, Or B. Barav, Bethan J. Jenkins, and Anthony H. Futerman. "Lysosomal Storage Disorders Shed Light on Lysosomal Dysfunction in Parkinson’s Disease." International Journal of Molecular Sciences 21, no. 14 (2020): 4966. http://dx.doi.org/10.3390/ijms21144966.

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The lysosome is a central player in the cell, acting as a clearing house for macromolecular degradation, but also plays a critical role in a variety of additional metabolic and regulatory processes. The lysosome has recently attracted the attention of neurobiologists and neurologists since a number of neurological diseases involve a lysosomal component. Among these is Parkinson’s disease (PD). While heterozygous and homozygous mutations in GBA1 are the highest genetic risk factor for PD, studies performed over the past decade have suggested that lysosomal loss of function is likely involved in
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Recla, Sabine, Andreas Hahn, and Christian Apitz. "Pulmonary arterial hypertension associated with impaired lysosomal endothelin-1 degradation." Cardiology in the Young 25, no. 4 (2014): 773–76. http://dx.doi.org/10.1017/s1047951114000997.

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AbstractWe report on a boy with severe pulmonary arterial hypertension associated with mucolipidosis, a rare lysosomal storage disorder. During diagnostic catheterisation, we found increased endothelin-1 levels, but normal big endothelin-1-levels (the precursor form of endothelin-1), which suggests impaired degradation of endothelin-1 rather than increased synthesis. As endothelin-1 degradation takes place in the lysosome, it appears likely that lysosomal dysfunction caused by the underlying disease contributes to the development of pulmonary arterial hypertension in this patient.
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Kavčič, Nežka, Katarina Pegan, and Boris Turk. "Lysosomes in programmed cell death pathways: from initiators to amplifiers." Biological Chemistry 398, no. 3 (2017): 289–301. http://dx.doi.org/10.1515/hsz-2016-0252.

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Abstract Lysosome is the central organelle for intracellular degradation of biological macromolecules and organelles. The material destined for degradation enters the lysosomes primarily via endocytosis, autophagy and phagocytosis, and is degraded through the concerted action of more than 50 lysosomal hydrolases. However, lysosomes are also linked with numerous other processes, including cell death, inflammasome activation and immune response, as well as with lysosomal secretion and cholesterol recycling. Among them programmed cell death pathways including apoptosis have received major attenti
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Dissertations / Theses on the topic "Lysosomale Degradation"

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Wegener, Elmar. "Modulierung der NF-KB-Aktivität in T-Zellen durch den Carmal1-Bcl10-Malt1 Komplex." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2006. http://dx.doi.org/10.18452/15507.

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Das Schicksal aktivierter T-Zellen wird durch eine Vielzahl NF-kappaB regulierter Ziel-Gene bestimmt, wobei aktivierende und deaktivierende Signale für die Ausbalancierung einer adäquaten T-Zell Antwort benötigt werden. Im Rahmen dieser Arbeit konnte gezeigt werden, dass die negativ-regulatorische Modulierung des Carma1-Bcl10-Malt1 (CBM)-Proteinkomplexes für die Steuerung der NF-kappaB Aktivität in T-Zellen von großer Bedeutung ist. Überraschenderweise ist die Bildung des CBM-Komplexes abhängig von IKKbeta, einer Kinase, die zuvor ausschließlich mit CBM-nachgelagerten Effektorfunktionen in Ver
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Ghislat, Cherfaoui Ghita. "Regulation of Lysosomal Degradation by CA2+And CA2+-Binding Proteins." Doctoral thesis, Universitat Politècnica de València, 2013. http://hdl.handle.net/10251/29690.

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La macroautofagia y la endocitosis son dos procesos catabólicos conservados evolutivamente en los que, mediante un tráfico vesicular, se degrada el material secuestrado, cuyo origen es intra- y extracelular, respectivamente. Ambos procesos comienzan de manera diferente: mediante la formación de un nuevo orgánulo, el autofagosoma, que secuestra material citoplásmico (macroautofagia), o mediante la internalización de material extracelular y de algunos componentes de la membrana plasmática a través de vesículas endocíticas (endocitosis). Sin embargo, los dos terminan en el mismo c
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Freeman, Craig. "The lysosomal degradation of heparan sulphate : a comparative study of the physical and catalytic properties of the heparan sulphate degradative enzymes /." Title page, contents and abstract only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09phf855.pdf.

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Pasquier, Adrien. "Lysosomal degradation of insulin granules promotes β-cell failure in type 2 diabetes". Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ083/document.

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Notre équipe a récemment découvert l’importance du ciblage des granules d’insuline aux lysosomes lors d’une mise à jeun chez les cellules pancréatiques β. Le diabète de type 2 (TD2) est caractérisé par la résistance à l’insuline couplé au dysfonctionnement des cellules β-et à leur perte. Je souhaitais évaluer le ciblage des granules d’insuline aux lysosomes dans le contexte diabétique. Grâce à un modèle murin, nous avons trouvé que le nombre des lysosomes contenant des granules d’insuline était augmenté chez les cellules β-provenant de souris diabétiques en comparaison aux contrôles. Ceci étai
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Mauri, Victor [Verfasser]. "Trehalose mediated enhancement of glycosaminoglycan degradation in the lysosomal storage disorder Mucopolysaccharidosis III / Victor Mauri." Köln : Deutsche Zentralbibliothek für Medizin, 2014. http://d-nb.info/1047324342/34.

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Adcocks, Clair. "An investigation into the roles of lysosomal proteinases, particularly cathepsin B, in cartilage proteoglycan degradation." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310755.

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Secker, Christopher [Verfasser]. "EGCG directly targets intracellular amyloid-β(1-42) aggregates and promotes their lysosomal degradation / Christopher Secker". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1179778847/34.

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Zasadny, Frederick Martin. "Lysosomal reacidification by degradation of poly(dl-lactide-CO-glycolide) nanoparticles in a lipotoxic cardiomyopathy model." Thesis, University of Iowa, 2016. https://ir.uiowa.edu/etd/2303.

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Lipotoxic cardiomyopathy increases the risk of heart failure in obese patients by adversely altering heart structure and function via toxic lipid specie mediated cellular stress and cell death. Increased fatty acid uptake and esterification in cardiomyocytes increases toxic lipid intermediates. These cardiotoxic lipid species such as diacylglycerol have recently been shown to deacidify lysosomes in cardiomyocytes by activating protein kinase C βII mediated NADPH oxidase 2 generation of superoxide that inhibits proton pumps on lysosomal membranes by S-nitrosylation. Autophagy, a lysosome depend
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Bala, Neeta. "AKAP200 promotes Notch stability by protecting it from Cbl/lysosome-mediated degradation in Drosophila." Thesis, Icahn School of Medicine at Mount Sinai, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10637108.

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<p>Cell signaling determines cellular behavior through the regulation of complex biochemical networks, slight disruptions in which can lead to a plethora of pathologies. The key to curing such diseases lies in part in gaining a comprehensive understanding of the mechanisms and molecules involved. The aim of this thesis was to characterize the role of A Kinase Anchoring Protein 200 (AKAP200), to expand our current understanding of signaling pathways in the context of development. AKAP200, a scaffolding protein previously known for its role in the spatial and temporal regulation of Protein Kinas
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Tran, Nguyen An Phu [Verfasser], and Olaf [Akademischer Betreuer] Riess. "Lysosomal degradation of alpha-Synuclein : Analysis in vivo and in vitro / An Phu Tran Nguyen ; Betreuer: Olaf Riess." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1163397067/34.

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Books on the topic "Lysosomale Degradation"

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Dice, J. Fred. Lysosomal Pathways of Protein Degradation. Landes Bioscience, 2000.

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Poorthuis, Ben. Lysosomal Storage Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0046.

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Lysosomal storage disorders are characterized by the presence of nondegraded material in endosomal / lysosomal compartments. Any process that interferes with the lysosomal degradation or endosomal / lysosomal transport of molecules can give rise to storage. The cause may be genetic in nature or environmental, as is the case in drug-induced lipidoses or when undegradable materials are present. In this chapter we discuss the genetic lysosomal storage disorders.
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Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, a
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Book chapters on the topic "Lysosomale Degradation"

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McCullough, John, Michael J. Clague, and Sylvie Urbé. "Ubiquitin and Protein Sorting to the Lysosome." In Protein Degradation. Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527620227.ch4.

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Chatterjee, R., M. Lones, and G. Kalnitsky. "Histone degradation by lysosomal proteases." In Cysteine Proteinases and their Inhibitors, edited by Vito Turk. De Gruyter, 1986. http://dx.doi.org/10.1515/9783110846836-015.

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Kirschke, H., J. Langner, S. Riemann, B. Wiederanders, S. Ansorge, and P. Bohley. "Lysosomal Cysteine Proteinases." In Ciba Foundation Symposium 75 - Protein Degradation in Health and Disease. John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720585.ch2.

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Hancock, Larry W., and Glyn Dawson. "Lysosomal Degradation of Glycoproteins and Glycosaminoglycans." In Neurobiology of Glycoconjugates. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-5955-6_6.

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Terman, Alexei, and Ulf T. Brunk. "Aging and Lysosomal Degradation of Cellular Constituents." In Aging at the Molecular Level. Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0667-4_15.

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Freeman, Craig, and John Hopwood. "Lysosomal Degradation of Heparin and Heparan Sulphate." In Advances in Experimental Medicine and Biology. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-2444-5_13.

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Barrett, Alan J. "Cathepsin D: The Lysosomal Aspartic Proteinase." In Ciba Foundation Symposium 75 - Protein Degradation in Health and Disease. John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720585.ch3.

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Conzelmann, Ernst, Mary Lee-Vaupel, and Konrad Sandhoff. "The Physiological Roles of Activator Proteins for Lysosomal Glycolipid Degradation." In Lipid Storage Disorders. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1029-7_39.

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Fridkin, Mati, Oren Rosen, Ronald Anderson, Frederick C. de Beer, and Enid G. Shephard. "Degradation of C-reactive protein (CRP) by neutrophil lysosomal enzymes generates peptidic neutrophil modulators." In Peptides 1990. Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3034-9_368.

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Dice, J. F., H. L. Chiang, S. R. Terlecky, and T. S. Olson. "A Role for the 73-kDa Heat Shock Cognate Protein in a Lysosomal Pathway of Intracellular Protein Degradation." In Heat Shock. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76679-4_20.

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Conference papers on the topic "Lysosomale Degradation"

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Hong, Jaewoo, P. Charles Lin, Todd Wuest, and Yongfen Min. "Abstract 2655: Oxygen tension regulates lysosomal activation and receptor tyrosine kinase degradation." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2655.

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Hong, Jaewoo, P. Charles Lin, Todd Wuest, and Yongfen Min. "Abstract 2655: Oxygen tension regulates lysosomal activation and receptor tyrosine kinase degradation." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2655.

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Ding, Rui, Barton A. Kamen, Jia Shi, and Kathleen W. Scotto. "Abstract 992: Regulation of ABCG2 lysosomal degradation by xanthines: Role of the PI3K/AKT pathway." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-992.

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Li, Hewang, Peiying Yu, Robin A. Felder, Ammasi Periasamy, and Pedro A. Jose. "Angiotensin II-induced angiotensin II type I receptor lysosomal degradation studied by fluorescence lifetime imaging microscopy." In SPIE BiOS: Biomedical Optics, edited by Ammasi Periasamy and Peter T. C. So. SPIE, 2009. http://dx.doi.org/10.1117/12.811032.

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Zhang, Yan, Xuexiang Du, Mingyue Liu, et al. "Abstract B3: Hijacking antibody-induced CTLA-4 lysosomal degradation for safer and more effective cancer immunotherapy." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b3.

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Tanimoto, Ryuta, Chiara Palladino, Simone Buraschi, et al. "Abstract 1344: Progranulin promotes ubiquitination, sorting and lysosomal degradation of sortilin in castration-resistant prostate cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1344.

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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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Jeong, Soyeon, Kaipeng Jing, Soyeon Shin, et al. "Abstract 4651: Docosahexaenoic acid-induced degradation of epidermal growth factor receptor through lysosome and ubiquitin/proteasomal system in human non-small cell lung cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4651.

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Reports on the topic "Lysosomale Degradation"

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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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