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Dissertations / Theses on the topic 'Cell death pathways'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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1

McComb, Scott. "The Paradoxical Roles of Cell Death Pathways in Immune Cells." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24331.

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Cell death plays a vital role throughout the immune response, from the onset of inflammation to the elimination of primed T cells. Understanding the regulation of cell death within immune cells is of vital importance to understanding the immune system and developing therapies against various immune-disorders. In this thesis I have investigated the regulation of cell death and its functional role in of the innate and adaptive arms of the immune system. The mechanisms that govern expansion and contraction of antigen stimulated CD8+ T cells are not well understood. In the first section of this

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2

Yung, Hong Wa. "Regulation of astrocyte cell death by kinase signalling pathways." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620576.

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3

Mässenhausen, Anne von, Wulf Tonnus, and Andreas Linkermann. "Cell Death Pathways Drive Necroinflammation during Acute Kidney Injury." Karger, 2018. https://tud.qucosa.de/id/qucosa%3A71624.

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Renal tubules represent an intercellular unit and function as a syncytium. When acute tubular necrosis was first visualized to occur through a process of synchronized regulated necrosis (SRN) in handpicked primary renal tubules, it became obvious that SRN actually promotes nephron loss. This realization adds to our current understanding of acute kidney injury (AKI)-chronic kidney disease (CKD) transition and argues for the prevention of AKI episodes to prevent CKD progression. Because SRN is triggered by necroptosis and executed by ferroptosis, 2 recently identified signaling pathways of regul

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4

Guo, Jing. "Studying the signaling pathways in ROS-induced neuronal cell death /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20GUO.

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5

Benford, Helena L. "Molecular pathways of bisphosphonate-induced apoptosis." Thesis, University of Aberdeen, 2000. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602025.

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Recent studies have proposed that non-nitrogen-containing and nitrogen- containing bisphosphonate drugs inhibit osteoclastic bone resorption by different molecular mechanisms. The aim of this thesis was to investigate the molecular mechanisms of action of bisphosphonates in macrophages and osteoclasts and, in particular, the activation of caspase proteases and their role in apoptotic cell death. Apoptosis of J774 macrophages induced by nitrogen-containing bisphosphonates was found to involve the activation of caspase-3. By contrast, non-nitrogen- containing bisphosphonates did not cause caspas

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6

Zhang, Tongli. "Mathematical Models of Some Signaling Pathways Regulating Cell Survival and Death." Diss., Virginia Tech, 2008. http://hdl.handle.net/10919/29443.

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In a multi-cellular organism, cells constantly receive signals on their internal condition and surrounding environment. In response to various signals, cells proliferate, move around or even undergo suicide. The signal-response is controlled by complex molecular machinery, understanding of which is an important goal of basic molecular biological research. Such understanding is also valuable for clinical application, since lethal diseases like cancer show maladaptive responses to growth-regulating signals. Because the multiple feedbacks in the molecular regulatory machinery obscure cause-effect

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7

Yatim, Nader. "Coordinated activation of cell death and inflammatory pathways in dying cells regulate adaptive immunity." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC233.

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Les Cellules mourantes initient l'immunité adaptative en fournissant des stimuli inflammatoires et des antigènes pour les cellules dendritiques (CD), qui à leurs tour activent les cellules T CD8 + par un processus appelé la présentation-croisée. Pour définir comment les différentes formes programmées de la mort cellulaire influencent l'immunité, nous avions établi des modèles de nécroptose et apoptose, par l'activation spécifique de RIPK3 ou CASP8, que nous avons utilisé pour évaluer in vitro et in vivo la réponse immunitaire. Nous avons alors trouvé que les cellules nécroptotiques exprimant l

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8

Janson, Veronica. "Cisplatin-resistance and cell death in malignant pleural mesothelioma cells." Doctoral thesis, Umeå universitet, Medicinsk biovetenskap, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1680.

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Malignant pleural mesothelioma (MPM) is an aggressive, treatment-resistant tumour. Cisplatin (cis-diamminedichloroplatinum (II)) is the best single-agent chemotherapy for MPM, but platinum-based combination therapies give the best overall response rates. However, cisplatin use is limited by resistance and severe side effects. This thesis has increased the knowledge concerning cisplatin-induced cell death in MPM by describing a novel potential therapeutic target, and three novel phenotypes of cisplatin-resistance in a human MPM cell line (P31) and its cisplatin-resistant sub-line (P31res1.2). T

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9

Davies, Carwyn Children's Cancer Institute Australia for Medical Research UNSW. "The influence of p21WAF1 on cell death pathways in acute lymphoblastic leukaemia." Publisher:University of New South Wales. Children's Cancer Institute Australia for Medical Research, 2009. http://handle.unsw.edu.au/1959.4/44416.

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The p53 protein is a primary mediator of apoptosis and growth arrest after exposure to DNA-damaging agents. Previous work has categorised a wild type p53 gene in the majority of childhood acute lymphoblastic leukaemia (ALL) cases, in which instance the p53 protein functions as a modulator of chemotherapy-induced cell death. In contrast, certain p53-induced proteins, such as p21WAF1, can act in an anti-apoptotic manner, and bestow resistance to chemotherapy. Previous studies of the p53 pathway in ALL have utilised cell lines and primary material. In this study a model of ALL was utilised that h

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10

Zhang, Tejia. "Discovery of bioactive lipids and lipid pathways in cell death and disease." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11483.

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Apoptosis is an intricately regulated cellular process required for the health and homeostasis of living systems. The mitochondrial apoptotic pathway depends on the BCL-2 family of pro- and anti-apoptotic members whose interactions regulate cell fate. BAX and BAK are key pro-apoptotic proteins required for mitochondrial permeabilization during apoptosis. While the mitochondrial death program relies heavily on its protein components, evidences support equally crucial roles for lipids and lipid metabolism in promoting or hindering apoptosis at the mitochondria. To gain insight into the inter

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11

Chakraborty, Sayantan [Verfasser], and Barbara [Akademischer Betreuer] Conradt. "Novel roles of the central cell death pathway and cell corpse engulfment pathways in C. elegans / Sayantan Chakraborty. Betreuer: Barbara Conradt." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1100396004/34.

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12

Thakker, Parva. "T Cell Intrinsic and Extrinsic Role of XIAP, During CD8 T Cell Response Against Intracellular Pathogens." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42419.

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The magnitude and effectiveness of CD8 response against intracellular pathogens is directed by survival and apoptotic signals that govern the fate of T cells. XIAP is a bona fide endogenous inhibitor of apoptotic signals. In this thesis, I have investigated the role of XIAP at various stages of CD8 T cell response. I used both in vivo and in vitro models to show that XIAP acts in a CD8 T cell extrinsic and intrinsic manner to regulate the expansion and contraction phases of the CD8 T cell response, respectively. During the expansion phase, XIAP prevents the cell death of APCs to promote APC-

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13

Haseroth, Elke [Verfasser]. "Cell death pathways in the photodynamic therapy of hepatocellular carcinoma cells with tetrasulfonated aluminum phthalocyanine / Elke Haseroth." Ulm : Universität Ulm. Medizinische Fakultät, 2016. http://d-nb.info/1081456663/34.

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14

Popescu, Bogdan O. "Cell death and signal transduction pathways in Alzheimer's disease: the role of presenilin 1 /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-786-X/.

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15

Alotaibi, Moureq. "CELL DEATH AND GROWTH ARREST PATHWAYS MEDIATING THE ACTIONS OF STILBENE 5C IN HCT-116 COLON CANCER CELLS." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2851.

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Abstract The stilbene derivative, cis-3, 4’, 5-trimethoxy-3’-aminostilbene (stilbene 5c), is a potentially potent antitumor agent that acts via binding to the colchicine-binding pocket in microtubules. Earlier studies have shown that stilbene 5c induces cell death in ovarian cancer cells and leukemic cells. The present study was designed to investigate the effectiveness of this microtubule poison against the HCT-116 human colon cancer cell line and its mechanisms of action. Time course studies demonstrated that stilbene 5c produces a biphasic decrease in cell viability. The capacity of the ce

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16

Senaratne, Siddhika Gaurie. "Action and interaction of various drugs with signal transduction pathways, leading to cancer cell death." Thesis, St George's, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398083.

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17

Heywood, Darren J. "Investigating the involvement of the JNK and PKC signalling pathways in mediating neuronal cell death." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288333.

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18

Glover, Colin P. J. "Optimization of gene transfer systems to facilitate studies investigating transcriptional pathways mediating neuronal cell death." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274633.

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19

Venables, Luanne. "In vitro induction of cell death pathways by artemisia afra extract and isolation of an active compound, isoalantolactone." Thesis, Nelson Mandela Metropolitan University, 2014. http://hdl.handle.net/10948/d1021087.

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Artemisia afra is one of the oldest, most well known and widely used traditional medicinal plants in South Africa. It is used to treat many different medical conditions, particularly respiratory and inflammatory ailments. There is no reported evidence of its use for the treatment of cancer but due to its reported cytotoxicity, an investigation of the mode of cell death induced by an ethanol A. afra extract using two cancer cell lines was done. IC50 values of 18.21 and 31.88 μg/mL of ethanol extracts were determined against U937 and HeLa cancer cells, respectively. An IC50 value of the aqueous

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20

Sathasivam, Sivakumar. "Investigation of cell death pathways in a cell culture model of Cu/Zn superoxide dismutase-related familial motor neurone disease." Thesis, University of Sheffield, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412435.

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21

Maya-Pineda, Héctor Rubén. "Sensitization of prostate cancer cells to cytotoxic drugs induced by the small adenoviral E1A12S protein through multiple cell death/signalling pathways." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8482.

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Replication-selective oncolytic adenoviruses represent a promising anticancer approach with proven efficacy in cancer cell lines and tumour xenografts in vivo. Anti-tumour efficacy, both in preclinical studies and clinical trials, was significantly improved in combination with chemotherapeutics in numerous cancers, including prostate cancer. It has been established that expression of the viral E1A gene is essential for the enhancement of cell killing in combination with cytotoxic drugs. The overall goal of this project is to identify specific E1A gene regions involved in the sensitization to t

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22

Zimmermann, Angela K. "A novel mechanism underlying BCL-2 antioxidant function : its role in mitochondrial apoptotic pathways and virus-induced neuronal cell death /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Neuroscience) -- University of Colorado Denver, 2007.<br>Typescript. Includes bibliographical references (leaves 140-162). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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23

DeMasters, Gerald Alan. "Influence of the Vitamin D3 Analog EB 1089 on Senescence and Cell Death Pathways in the Response of Breast Tumor Cells to Ionizing Radiation." Abstract, 24-page preview and downloadable full-text (PDF format) available to VCU users at:, 2006. http://hdl.handle.net/10156/1620.

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24

Lema, Asqui Saúl Stalin. "Pathogen-triggered programmed cell death in plants: Metacaspase 1-dependent pathways = Muerte celular programada desencadenada por patógenos en plantas: vías dependientes de Metacaspasa 1." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/586256.

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The hypersensitive response (HR) is a paradigmatic type of programmed cell death, that occurs in response to pathogen recognition at the site of attempted invasion. Notwithstanding more than a century of research on HR, many are the aspect that are still unknown about how it is so tightly regulated and how it can be contained spatially to a few cells. The hypersensitive response in the Arabidopsis thaliana is controlled by type I metacaspase AtMC1 which is a positive regulator of pathogen-triggered PCD and autophagy, and that negative regulation of AtMC1 by AtLSD1 or AtMC2 can prevent runaway

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25

Abrantes, Julia Laura Fernandes 1984. "Expressão ectópica de miR-34a em células de melanoma metastático humano = efeitos sobre vias de sinalização relacionadas com sobrevivência, proliferação e morte celular = Ectopic expression of miR-34a in human metastatic melanoma cells: effects on signaling pathways related to survival, proliferation and cell death." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314040.

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Orientador: Carmen Veríssima Ferreira Halder<br>Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia<br>Made available in DSpace on 2018-08-22T16:08:32Z (GMT). No. of bitstreams: 1 Abrantes_JuliaLauraFernandes_D.pdf: 4562084 bytes, checksum: fba9dbca16cd31c006b311ff23a0b41b (MD5) Previous issue date: 2013<br>Resumo: O melanoma é o tipo mais agressivo de câncer de pele. Seu tratamento permanece como um grande desafio, já que em estágio avançado torna-se extremamente refratário aos tratamentos convencionais. miR-34a é um microRNA supressor de tumor com expressão normalme

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26

Palmer, Daniel Harrison. "A study of the novel VDEPT cancer gene therapy combination nitroreductase / CB1954 : mechanisms of cell death, modulation of cellular signalling pathways and early phase clinical trials." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403904.

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A major limitation to the success of cancer gene therapy is the low efficiency of gene delivery achieved by currently available vectors. Virus-directed enzyme prodrug therapy aims to overcome this limitation by delivery of an enzyme to the tumour site, which catalyses the conversion of an inert prodrug to a potent cytotoxic. Activation of the prodrug at the tumour site maximises local cell kill whilst minimising systemic toxicity. Importantly, the activated species should pass to neighbouring nontransduced cells to mediate 'bystander' killing. In this way, significant anti-tumour effects may b

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27

Dallimore, Elizabeth Jane. "Molecular and cellular characteristics of early vs late born retinal ganglion cells." University of Western Australia. School of Anatomy and Human Biology, 2009. http://theses.library.uwa.edu.au/adt-WU2009.0138.

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[Truncated abstract] Developmentally, the rodent retinocollicular projection is often thought of as a homogenous projection of retinal ganglion cell (RGC) axons, however the extensive period of RGC neurogenesis and sequential arrival of their axons into central targets such as the superior colliulus (SC) suggests otherwise. RGC axons are already present in the developing SC at embryonic (E) day 16.5-17. RGCs born on E15 have innervated the SC by birth, whereas axons derived from RGCs that are born last (E19) do not grow into the SC until postnatal (P) days 4-6 (Dallimore et al., 2002). These o

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28

Akizuki, Mayumi. "Optineurin suppression causes neuronal cell death via NF-κB pathway". Kyoto University, 2014. http://hdl.handle.net/2433/188648.

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29

Abdo, Michael A. "Tumour necrosis factor : alpha signal transduction in rat corpus luteum apoptosis." University of Western Australia. School of Anatomy and Human Biology, 2002. http://theses.library.uwa.edu.au/adt-WU2003.0024.

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[Formulae and special characters can only be approximated here. Please see the pdf version of the abstract for an accurate reproduction.] Apoptosis is a morphologically distinct form of cell death that is involved in the regulation of normal and aberrant cell systems. The complexities of the apoptotic cell death pathway arise from variation in both the cellular specialisation and initial stimulus. The corpus luteum (CL) is an endocrine gland that whilst critical to the maintenance of pregnancy in the rat, regresses at the completion of each oestrous cycle and pregnancy. This regression is fa

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30

Rajamani, Uthra. "Hyperglycemia-induced activation of the hexosamine biosynthetic pathway causes myocardial cell death." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/1142.

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Thesis (PhD (Physiological Sciences))--University of Stellenbosch, 2009.<br>ENGLISH ABSTRACT: OBJECTIVE – Oxidative stress increases flux through the hexosamine biosynthetic pathway (HBP) resulting in greater O-GlcNAcylation of target proteins. Since increased oxidative stress and HBP flux are associated with insulin resistance, we hypothesized that its activation leads to greater O-GlcNAcylation of BAD (pro-apoptotic) and increased myocardial apoptosis. RESEARCH DESIGN AND METHODS – To investigate our hypothesis, we employed two experimental models: 1) H9c2 cardiomyoblasts exposed to hig

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31

O'Kane, H. F. "The FAS death receptor pathway in transitional cell carcinoma of the bladder." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426738.

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32

Wardle, Fiona Claire. "Regulation of the BMP signalling pathway by BMP-1 related metalloproteases." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287477.

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33

Andrusiak, Matthew. "Differential Roles for the Retinoblastoma Protein in Cycling and Quiescent Neural Populations." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24037.

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While the genetics of retinoblastoma and the implications of the retinoblastoma susceptibility gene, RB1, are well described, there is still scarce evidence to suggest why RB1 acts in such a cell-type specific manner. Using the murine cortex as a model, we examined the effects of RB1 deletion of cycling neural progenitors and post-mitotic neurons, in order to ascertain cell-type specific functions in the central nervous system. Using the previously identified cell-cycle independent role for Rb in tangential migration, we validated Rb/E2f regulation of neogenin and implicated it in this process

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34

Mbah, Nneka Elizabeth. "Defining the Mechanism of Methuosis, a Non-apoptotic Cell Death Pathway, Induced by Indolyl Chalcone Compounds in Glioblastoma Cells." University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1481303173869378.

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35

Darling, Nicola Jane. "Regulation of ER stress-induced cell death by the ERK1/2 signalling pathway." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708709.

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Park, Yoo Jin. "The role of Fas-mediated apoptotic pathway in amyloid-induced beta-cell death." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52420.

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In type 2 diabetes (T2D), progressive dysfunction and loss of beta-cells in pancreatic islets eventually leads to hyperglycemia. The formation of toxic protein aggregates known as islet amyloid contributes to beta-cell dysfunction and death in T2D. Islet amyloid is formed mainly by aggregation of the beta-cell hormone named islet amyloid polypeptide (IAPP), which is produced and released along with insulin. Amyloid also forms in cultured and transplanted human islets, indicating that in addition to its role in pathogenesis of T2D, amyloid formation contributes to islet graft failure in type 1

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Wong, Helen Yunshan. "The role of mitochondrial (intrinsic) apoptotic pathway in hIAPP mediated β-cell death". Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58846.

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The full abstract for this thesis is available in the body of the thesis, and will be available when the embargo expires.<br>Medicine, Faculty of<br>Experimental Medicine, Division of<br>Medicine, Department of<br>Graduate

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Lam, Wun. "A screen for genetic modifiers of polyglutamine pathology in Drosophila implicates a Dronc-related pathway in polyglutamine-induced cell death." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611432.

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Crichton, Jennifer E. "The Role of the E3-ubiquitin Ligase Trim17 in the Mitochondrial Cell Death Pathway." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23715.

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The upregulation of apoptosis is a hallmark of several neurodegenerative disorders including ischemic stroke. In neurons, as in other cell types, Bax and tBid are critical regulators of the intrinsic pathway upstream of mitochondrial outer membrane permeabilization (MOMP) and caspase activation. The characterization of the molecular events that occur during the early stages is therefore extremely important from a therapeutic standpoint. Here I show that two independent genetic pilot screens looking for novel regulators of Bax activation identified a common hit in the E3 ubiquitin ligase Trim17

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Yu-Sheng, Yeh. "Studies on the role of cholesterol biosynthesis pathway on differentiation, cell death, and metabolism in adipocytes." Kyoto University, 2019. http://hdl.handle.net/2433/242687.

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Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(農学)<br>甲第21810号<br>農博第2323号<br>新制||農||1066(附属図書館)<br>学位論文||H31||N5182(農学部図書室)<br>京都大学大学院農学研究科食品生物科学専攻<br>(主査)教授入江一浩, 教授橋本渉, 准教授後藤剛<br>学位規則第4条第1項該当

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Britt, Erin L. "Targeting BCL-2 Family Members in the Cell Death Pathway to Treat Head and Neck Cancer." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5352.

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Head and neck cancer accounts for approximately 3 percent of all cancers in the United States, and over 90% of them are head and neck squamous cell carcinoma (HNSCC). Chemotherapeutic drugs that treat HNSCC can activate BCL-2 family dependent apoptosis. Pro-apoptotic NOXA induced by adenovirus (Ad-NOXA) or fenretinide inactivates anti-apoptotic MCL-1, while ABT-263 can inactivate other anti-apoptotic BCL-2 family members such as BCL-2 and BCL-XL. We used p53 inactive HN8 and HN12, p53 wild-type UMSCC1, and HPV-positive UMSCC47 human HNSCC cell lines and five mouse HNSCC cell lines. Cells were

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Wise, Randi. "The role of the secretory pathway and cell surface proteolysis in the regulation of the aggressiveness of breast cancer cells." Diss., Kansas State University, 2017. http://hdl.handle.net/2097/38199.

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Doctor of Philosophy<br>Biochemistry and Molecular Biophysics Interdepartmental Program<br>Anna Zolkiewska<br>Cancer cells exploit key signaling pathways in order to survive, proliferate, and metastasize. Understanding the intricacies of the aberrant signaling in cancer may provide new insight into how to therapeutically target tumor cells. The goal of my research was to explore the role of two modulators of transmembrane signaling, the secretory pathway and cell surface proteolysis, in the aggressiveness of breast cancer cells. To study the role of the secretory pathway, I focused on the fami

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Matsumoto, Yoshihide. "Epithelial EP4 plays an essential role in maintaining homeostasis in colon." Kyoto University, 2020. http://hdl.handle.net/2433/253165.

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Kwon, Jungeun Sarah, Nicholas J. Everetts, Xia Wang, et al. "Controlling Depth of Cellular Quiescence by an Rb-E2F Network Switch." CELL PRESS, 2017. http://hdl.handle.net/10150/625987.

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Quiescence is a non-proliferative cellular state that is critical to tissue repair and regeneration. Although often described as the G0 phase, quiescence is not a single homogeneous state. As cells remain quiescent for longer durations, they move progressively deeper and display a reduced sensitivity to growth signals. Deep quiescent cells, unlike senescent cells, can still re-enter the cell cycle under physiological conditions. Mechanisms controlling quiescence depth are poorly understood, representing a currently underappreciated layer of complexity in growth control. Here, we show that the

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Evans, A. K. C. "The role of the programmed cell death (PD-1) pathway in the immunopathogenesis of chronic hepatitis B infection." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1138759/.

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Chronic hepatitis B (CHB) results from a complex interaction between a replicating non-cytopathic virus and an impaired antiviral host immune response. The Programmed Cell Death (PD-1) pathway is an immunoinhibitory T-cell pathway implicated in virus-specific T-cell dysfunction in several chronic viral infections. The role of the PD-1 pathway in the immunopathogenesis of chronic hepatitis B was investigated through several different approaches. Firstly, longitudinal changes in PD-1 expression in patients with CHB undergoing oral antiviral therapy was investigated. A direct correlation between

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Sharma, Deepa [Verfasser], and Erich [Akademischer Betreuer] Gulbins. "Regulation and function of acid sphingomyelinase (ASM)/ceramide pathway in irradiation-induced cell death / Deepa Sharma. Betreuer: Erich Gulbins." Duisburg, 2015. http://d-nb.info/1079182489/34.

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Chang, Samantha J. "p53, CLIC, AND THE JAK/STAT PATHWAY: INVESTIGATING THE LINK BETWEEN CANCER STRESSES AND CELL DEATH IN DROSOPHILA MELANOGASTER." Ohio University Honors Tutorial College / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1399820564.

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48

Fraser, Alison. "An investigation of the cellular responses to the unsymmetrically substituted polyamine analogues and identification of the pathway to cell death." Thesis, University of Aberdeen, 2003. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602324.

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HL-60 human promyelogenous leukaemic cells were used as a model to determine the cytotoxic potential of the unsymmetrically substituted polyamine analogues CHENSpm, CPENSpm and IPENSpm with a view to their use as chemotherapeutic agents. The cytotoxicity was compared with etoposide, an established cytotoxic drug. The analogues CHENSpm and IPENSpm induced cytotoxicity over 48 h, with decreases in cell number and protein content, with CPENSpm showing a growth inhibitory effect after 96 h. The cellular content of all 3 polyamines was decreased in all treatments, and this resulted from increases i

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Turnbull, Stuart. "The central role of a metal-protein aggregation-dependent oxidative stress pathway in the pathogenesis of cell death in neurodegenerative diseases." Thesis, Lancaster University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413793.

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Chen, Szu-ying, and 陳思穎. "Signaling pathways of caspase inhibitor induced cell death." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/70347502503671890314.

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碩士<br>國立臺灣大學<br>藥理學研究所<br>96<br>Benzyloxycarbonyl-Val-Ala-Asp (ZVAD), a pancaspase inhibitor has been widely used to abolish apoptotic cell death. Interestingly, previous reports showed that ZVAD alone induces necrosis accompanying with autophagosome formation, which termed as autophagic cell death, in L929 fibrosarcoma cells. They found that ZVAD-induced autophagic cell necrosis relies on caspase 8 inhibition, RIP1, JNK activity, and ROS accumulation. Until now the connection of these molecules and signaling mechanisms in details, however, are unclear. Therefore the aim of this study is to el

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