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Dissertations / Theses on the topic 'Lysosomale Degradation'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Humphries, William Henry IV. "Intracellular degradation of low-density lipoprotein probed with two-color fluorescence microscopy." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/42832.

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The vesicle-mediated degradation of low-density lipoprotein (LDL) is an essential cellular function due to its role in cellular biosynthesis of membranes and steroids. Using multi-color single particle tracking fluorescence microscopy, the intracellular degradation of LDL was probed in live, intact cells. Unique to these experiments is the direct observation of LDL degradation using an LDL-based probe that increases fluorescence intensity upon degradation. Specifically, individual LDL particles were labeled with multiple fluorophores resulting in a quenched fluorescent signal. The characterist

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12

Bolt, Alicia Marie. "Arsenite Alters Lysosome-Mediated Degradation and the Autophagy Process Leading to Immunosuppression in Human B-Lymphoblastoid Cell Lines." Diss., The University of Arizona, 2012. http://hdl.handle.net/10150/222895.

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The immune system is a target of arsenic toxicity. Epidemiological data have shown that arsenic exposure is associated with characteristics of immunosuppression. Human B-lymphoblastoid cell lines (LCL) were used as an in vitro model of immune cell targeting by arsenic to investigate the mechanism of arsenic-induced cytotoxicity, which could provided insight into the mechanism underlying arsenic-induced immunotoxicity leading to the immunosuppression observed in humans. In LCL arsenite-induced cytotoxicity was not associated with apoptosis, but associated with hallmarks of autophagy, a cell st

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13

BALAVOINE, SOPHIE. "Degradation des arn ribosomaux dans les hepatocytes de rat isoles et en culture primaire : regulation par les acides amines et l'insuline. role du systeme lysosomal." Paris 7, 1993. http://www.theses.fr/1993PA077009.

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La degradation des arn ribosomaux (arnr) par les acides amines et l'insuline a ete etudiee dans les hepatocytes isoles et en culture primaire provenant de rats nourris ad libitum. La vitesse de degradation des arnr a ete determinee a partir de l'accumulation de cytidine radioactive dans le milieu de suspension ou de culture, en presence de 0,5 mm de cytidine non radioactive. Les arnr ont ete marques in vivo par l'acide 6-#1#4corotique 60 h avant l'isolement des hepatocytes. Lorsque les hepatocytes etaient maintenus dans un milieu depourvu en acides amines, les arnr etaient degrades a une vites

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14

Lööv, Camilla. "Cellular and Molecular Responses to Traumatic Brain Injury." Doctoral thesis, Uppsala universitet, Neurokirurgi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-215154.

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Traumatic brain injury (TBI) is a relatively unknown disease considering the tens of millions of people affected around the world each year. Many TBI patients die from their injuries and survivors often suffer from life-long disabilities. The primary injury initiates a variety of cellular and molecular processes that are both beneficial and detrimental for the brain, but that are not fully understood. The focus of this thesis has been to study the role of astrocytes in clearance of dead cells after TBI and to identify injury specific proteins that may function as biomarkers, by using cell cult

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15

Dias, Roberto Alexandre dos Santos. "Characterization of Gαo role on neuritogenesis: a focus on the Gαo-Amyloid precursor protein complex". Doctoral thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22057.

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Doutoramento em Biomedicina<br>Gαo is the most abundant Gα subunit present in the brain, however, its specific functions are still far from clear. Studies of the signaling pathways modulated by Gαo have uncovered potential roles for Gαo in the development of the nervous system, especially in neuritogenesis. The characterization of Gαo interactome has also been crucial for the better understanding of this protein’s functions. One of the Gαo interacting proteins is the amyloid precursor protein (APP), a protein that is involved in several physiological functions, such as cell survival, neu

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16

Miles, Anna Louise. "V-ATPase regulation of Hypoxia Inducible transcription Factors." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/283217.

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Metazoans have evolved conserved mechanisms to promote cell survival under low oxygen tensions by initiating a transcriptional cascade centered on the action of Hypoxia Inducible transcription Factors (HIFs). In aerobic conditions, HIFs are inactivated by ubiquitin-proteasome-mediated degradation of their a subunit, which is dependent on prolyl hydroxylation by 2-oxoglutarate (2-OG) and Fe(II)-dependent prolyl hydroxylases (PHDs). In hypoxia, HIF-$\alpha$ is no longer hydroxylated and is therefore stabilised, activating a global transcriptional response to ensure cell survival. Interestingly,

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17

Tavares, Lucas Alves. "O envolvimento da proteína adaptadora 1 (AP-1) no mecanismo de regulação negativa do receptor CD4 por Nef de HIV-1." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-06012017-113215/.

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O Vírus da Imunodeficiência Humana (HIV) é o agente etiológico da Síndrome da Imunodeficiência Adquirida (AIDS). A AIDS é uma doença de distribuição mundial, e estima-se que existam atualmente pelo menos 36,9 milhões de pessoas infectadas com o vírus. Durante o seu ciclo replicativo, o HIV promove diversas alterações na fisiologia da célula hospedeira a fim de promover sua sobrevivência e potencializar a replicação. A rápida progressão da infecção pelo HIV-1 em humanos e em modelos animais está intimamente ligada à função da proteína acessória Nef. Dentre as diversas ações de Nef está a regula

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18

Tsai, Chi-Hua, and 蔡奇樺. "Proteasome inhibitors overcome lapatinib resistance through lysosomal degradation of HER family." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/x98tcc.

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碩士<br>中國醫藥大學<br>癌症生物學研究所碩士班<br>102<br>All members of HER family are frequently overexpressed in several human cancers of epithelial origin and play important roles in the development and progression of breast cancers. According to clinical statistics, approximately 25%–30% of human breast cancers overexpress HER2, and most of these cases are due to the amplification of c-HER2 proto-oncogene. Lapatinib, a dual EGFR/HER2 tyrosine kinase inhibitor, has shown significant clinical benefits in advanced HER2-positve breast cancer patients, but the response is not durable. Therefore, development of al

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19

Hsieh, Cheng-Wei, and 謝正偉. "Lysosome-responsive Transcription Factor EB Activation upon Mitophagy Degradation Stress." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/66573960627460377270.

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博士<br>國立清華大學<br>化學系<br>104<br>Except of the simplified view of lysosomes as the final compartments of degradation process, lysosomes are increasingly regarded as upstream organelles in the control of cell functions. Therefore, lysosome homeostasis should be tightly regulated to match the catabolic needs as well as to maintain lysosomal pathways. Here we use light-induced mitophagy substrates to disturb lysosome homeostatsis and reveal how lysosome biogenesis responses quantitatively to different levels of degradation stress. We observed that TFEB-mediated lysosomal genes activation is upregula

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20

Wang, Fan. "Modulating Protein Homeostasis to Ameliorate Lysosomal Storage Disorders." Thesis, 2012. http://hdl.handle.net/1911/64709.

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The goal of this project has been to develop therapeutic strategies for protein misfolding diseases caused by excessive degradation of misfolded proteins and loss of protein function. The focus for this work is lysosomal storage disorders (LSDs), a group of more than 50 known inherited metabolic diseases characterized by deficiency in hydrolytic enzymes and consequent buildup of lysosomal macromolecules. Gaucher’s Disease (GD) is used as a representative of the family of LSDs in this study. GD is caused by mutations in the gene encoding lysosomal glucocerebrosidase (GC) and consequent accumula

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21

Cho, Chia-Fong, and 卓家楓. "Kringle 1-5 of Plasminogen Downregulated Thrombomodulin Through Proteosome-Lysosome Degradation Pathway." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/95587374389221918345.

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碩士<br>國立成功大學<br>生物化學研究所<br>93<br>Angiogenesis plays an important role in many physiological and pathological processes, including embryonic vascular system development, wound healing, and reproductive cycle in adult female and tumorigenesis. Many reports indicate that cancer cells can secrete angiogenic factors to stimulate the growth of new blood vessels during the formation of tumor. Angiostatin, a proteolytic fragment of plasminogen, is a potent antagonist of angiogenesis and inhibitor of endothelial cell proliferation and migration. Thrombomodulin (TM) is a glycoprotein receptor and cofact

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22

Wu, Nan-Ying, and 吳南瑩. "Comparison of Skp2 degradation via proteasomal and lysosomal pathways in non-stressed and arsenite-treated cells." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/30745102777687735138.

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碩士<br>國立清華大學<br>生物科技研究所<br>96<br>Skp2 is an F-box protein of the Skp1-Cullin-F-box ubiquitin ligase complex that is responsible for degradation of Cyclin-dependent kinase inhibitors to timely control cell cycle progression. Skp2 degradation is known to be mediated via the APCCdh1-26S proteasome pathway during G0/G1 stage. Additionally, our previous study suggests that Skp2 degradation requires the activities of lysosomal proteases following arsenite stress. Here I explored the mechanisms of Skp2 degradation via proteasomal and lysosomal pathways in non-stressed and arsenite-treated cells. Two

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23

Palsamy, Kanagaraj. "Souffle/Spastizin regulates secretory granule maturation by sorting lysosomal cargo from immature secretory granule during zebrafish oogenesis." Doctoral thesis, 2014. http://hdl.handle.net/11858/00-1735-0000-0022-600E-5.

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24

Sandeepa, M. E. "Survival Strategies Of SALMONELLA." Thesis, 2008. http://hdl.handle.net/2005/840.

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The genus Salmonella includes facultative intracellular pathogens. Salmonella enterica serovar Typhi (S. Typhi) causes typhoid fever in humans killing about 2,00,000 people globally every year. Salmonella enterica serovars Typhimurium (S. Typhimurium) and Enteritidis (S. Enteritidis) cause food poisoning in humans. Salmonellae also cause disease in animals of economic importance like poultry and cattle. Treatment of diseases caused by these notorious pathogens is becoming more and more difficult because of the emergence of drug resistant strains. Thus, it is vital to understand the virulence m

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