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Tesis sobre el tema "Cell death"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

Pat, Sze Wa. "Cell metabolism in cell death and cell growth." HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.

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2

Crisby, Milita. "Cell death in atherosclerosis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3191-7/.

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3

Ellison, David William. "Cell proliferation, cell death, and differentiation in gliomas." Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295912.

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4

Uppington, Kay Marie. "Cell death in prion disease." Thesis, University of Bath, 2008. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488879.

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Prion diseases are a group of fatal neurodegenerative diseases, including CJD and scrapie, which are thought to be caused by a protein termed a prion (PrP). As manganese has previously been suggested to be involved in prion disease we have investigated manganese binding to PrP and its role in the toxicity of the protein. We have shown that manganese bound PrP (MnPrP) has several of the characteristics of the disease form of PrP, including protease resistance and toxicity that is dependent on cellular PrP expression. Further investigation into the mechanism of toxicity revealed that MnPrP is si

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5

Beeharry, Neil. "Cell death in insulin-containing cells : induction and prevention." Thesis, University of Brighton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401600.

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6

Gorak-Stolinska, Patricia. "Activation induced cell death in human T cell subsets." Thesis, King's College London (University of London), 2002. http://kclpure.kcl.ac.uk/portal/en/theses/activation-induced-cell-death-in-human-t-cell-subsets(eb708e24-eccb-42fc-8930-d62ddf6794c1).html.

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7

Cheng, Jade. "Regulation of cell division and cell death by GRASP65." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544414.

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8

RUNYAN, CHRISTOPHER MICHAEL. "The Role of Cell Death in Germ Cell Migration." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1210732680.

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9

Courtois-Moreau, Charleen Laetitia. "Programmed Cell Death in Xylem Development." Doctoral thesis, Umeå universitet, Umeå Plant Science Centre, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1831.

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Concerns about climate changes and scarcity of fossil fuels are rising. Hence wood is becoming an attractive source of renewable energy and raw material and these new dimensions have prompted increasing interest in wood formation in trees, in both the scientific community and wider public. In this thesis, the focus is on a key process in wood development: programmed cell death (PCD) in the development of xylem elements. Since secondary cell wall formation is dependent, inter alia, upon the life time of xylem elements, the qualitative features of wood will be affected by PCD in xylem, about whi

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10

Klassen, Shaun Scott. "Nitric oxide-induced cardiomyocyte cell death." Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/31539.

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Nitric oxide (NO), a regulator of diverse cardiovascular functions, modifies cardiac cell viability through mechanisms that remain uncertain. Several pathways were studied to understand these effects. The possibility that the protein p53 is involved in the cardiomyocyte response to the NO donor s-nitrosoglutathione (GSNO) or the peroxynitrite donor 3- morpholinosydnonimine (SIN-1) was explored. These donors induced a concentration-dependent increase of cell death in cultured embryonic chick cardiomyocytes. Expression of p53 protein was increased in response to GSNO, specifically in the n

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11

Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0025/MQ50832.pdf.

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12

Maianski, Nikolai. "Neutrophil cell death: mechanisms and regulation." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/88280.

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13

Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21605.

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Oxygen free radicals have been implicated in several diseases including ischemic stroke, and myocardial infarction. They can trigger chain reactions like peroxidation of membrane phospholipids, leading to osmotic imbalance and cell death. Isoprostanes are stable products of lipid peroxidation that have a constrictor effect on the vasculature and bronchii. As isoprostanes are abundantly generated in tissues under oxidant stress, we have hypothesized that they could be related to endothelial dysfunction observed during ischemia/reperfasion by affecting endothelial cell survival. The effects of 8

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14

Spanos, Sophia. "Cell death during preimplantation embryo development." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398228.

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15

Świdziński, Jodi A. "Programmed cell death in Arabidopsis thaliana." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:6e2580fc-8873-4722-89f7-b206d4be2a5f.

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Programmed Cell Death (PCD) describes an orderly cellular breakdown that occurs in both plants and animals throughout development and in response to biotic and abiotic stresses. The molecular machinery that functions in the induction and execution of animal PCD has been characterised in great detail. Conversely, few genes and proteins involved in plant PCD have been identified. While certain features of animal PCD may be conserved, the induction and execution of plant PCD is also likely to involve novel proteins and mechanisms. The aim of the work presented in this thesis was to investigate ex

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16

Cox, Orla T. "Vascular cell death in diabetic retinopathy." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343079.

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17

Sharma, Pundrique Radheyshyam. "Programmed cell death during heart development." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272255.

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18

Fitzgerald, Julia. "Monoamine oxidase in neuronal cell death." Thesis, Nottingham Trent University, 2008. http://irep.ntu.ac.uk/id/eprint/51/.

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Monoamine oxidase (MAO) is an oxidative enzyme that deaminates a variety of amine substrates, including the neurotransmitter dopamine. The enzymatic reaction requires molecular oxygen and produces hydrogen peroxide as a by-product. MAO is localised in the outer mitochondrial membrane and exists as two isoforms, MAO-A and MAO-B, which are differentially expressed in the body and differ in their substrate and inhibitor specificities. Previous studies have suggested that MAO-generated reactive oxygen species (ROS) contribute to oxidative stress in the cell and can directly inhibit electron transp

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19

Ramos, Paulina Joanna. "Fibronectin Enhances Carfilzomib Mediated Cell Death." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579327.

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Cell Adhesion Mediated Drug Resistance (CAM-DR) is a factor in Multiple Myeloma (MM) drug resistance. Despite advances in treatment, multiple myeloma remains incurable and often results in drug resistance. It is known that cell adhesion to fibronectin via integrin β1 confers survival in myeloma cells. We show here that adherence of the NCI-H929 and MM.1S myeloma cells to fibronectin, promotes cell death when treated with proteasome inhibitor Carfilzomib (Kyprolis). These data are in contrast to other cytotoxic drugs, such as melphalan or doxorubicin, and different myeloma cell lines in which t

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20

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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21

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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22

Kaul, Aparna. "Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells." University of Toledo Health Science Campus / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=mco1243364096.

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23

Koterba, Kristen L. "Regulation of Autophagy and Cell Death in Breast Carcinoma Cells." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1276005638.

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24

Stuckey, Crystal Elaine. "Oxidative Stress and Cell Death in Osmotically Swollen Glial Cells." Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1208492663.

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25

Prise, Kevin M. "Cell death and DNA damage in methotrexate-treated HeLa cells." Thesis, University of Aberdeen, 1985. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU362655.

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The cancer chemotherapeutic agent methotrexate inhibits the enzyme dihydrofolate reductase leading to a depletion of cellular reduced folates and inhibition of thymidylate synthase. A predicted consequence of this depletion of cellular thymidylate residues is that the nucleotide dUMP may be incorporated into DNA in place of dTMP. The subsequent cycle of uracil removal and reincorporation by an excision-repair pathway may cause DNA damage, a possible contributory factor leading ultimately to cell death. DNA. damage, in the form of single- and double-strand breaks, was -5 detected in HeLa cells

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26

Stuart, Lynda Maria. "Cell death, dendritic cells and downregulation of the immune response." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23214.

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Apoptotic cells are an important source of many autoantigens and the realization that dendritic cells (DCs), the main antigen presenting cell of the adaptive immune system, not only internalise such drying cells but present antigen derived from them had important implications for our understanding of autoimmunity, tumour immunology and anti-viral responses. The aim of this thesis was to explore the likely consequences of clearance of cells dying by constitutive apoptosis by myeloid phagocytes, with particular emphasis on the mechanism and outcome of DC clearance and the implications for autoim

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27

Ahmed, Yasser Abdel Galil. "Analysis of physiological death in equine chondrocytes /." Connect to thesis, 2007. http://eprints.unimelb.edu.au/archive/00003656.

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28

Jahnke, Ulrike. "Cell cycle de-regulation and cell death in leukaemia chemotherapy." Thesis, Queen Mary, University of London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439424.

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29

Watson, Andrea. "Heat shock proteins in leukaemia cell differentiation and cell death." Thesis, Aston University, 1990. http://publications.aston.ac.uk/12533/.

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When HL60 cells were induced to differentiate to granulocyte-like cells with the agents N-methylformamide and tunicamycin an concentrations marginally below those which were cytotoxic, there was a decrease in the synthesis of the glucose- regulated proteins which preceded the expression of markers of a differentiated phenotype. There was a transient increase in the amount of hsp70 after 36 hours in NMF treated cells but in differentiated cells negligible amounts were detected. Inducers which were known to modulate hsp70 such as azetadine carboxylic acid did not induce differentiation suggestin

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30

Sciacovelli, Marco. "Cell death regulation by mitochondrial chaperones in tumor cell models." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3421645.

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Cancer cells are endowed with the capability to evade normal apoptotic signaling, as they display a constitutive hyperactivation of kinase signaling pathways. Integration of survival and death stimuli occurs on mitochondria, where many of these signals converge in the regulation of a channel termed permeability transition pore (PTP). PTP opening commits cells to death, and it is regulated by a variety of factors, among which molecular chaperones play a pivotal role. Here I have studied how mitochondrial chaperones interact with signal transduction pathways, modulate the PTP and more in general

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31

Tamm, Christoffer. "Apoptotic cell death in neural stem cells exposed to toxic stimuli /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-301-6/.

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32

Ajabnoor, Ghada. "Mechanism of cell death in drug resistant human breast cancer cells." Thesis, University of Surrey, 2010. http://epubs.surrey.ac.uk/842867/.

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Anticancer drug resistance occurs as a result of altered response to cytotoxic insult, via inhibition or inactivation of apoptosis (programmed cell death type I, PCDI), which plays a major role in tumour development and progression. An alternative form of cell death - non-apoptotic, or autophagic cell death (PCD II) has recently emerged as a factor contributing to the cytotoxic response of cancer cells. We studied in vitro cell death in a drug resistant model MCF-7 human breast cancer cells with acquired resistance (c. 10- 20 fold) to paclitaxel, termed MCF-7TaxR. It has been reported that the

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33

Jaligam, Vanaja. "Developmental cell death in the midline glia cells of Drosophila embryo." College Park, Md. : University of Maryland, 2004. http://hdl.handle.net/1903/1467.

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Thesis (M.S.) -- University of Maryland, College Park, 2004.<br>Thesis research directed by: Dept. of Cell Biology and Molecular Genetics. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.

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34

Wilkie, Alexander David. "Evasion of Cell Death in Burkitt’s Lymphoma and Pancreatic Cancer Cells." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367897.

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This thesis examined exploitation of cell death to combat cancer from two angles: investigating cell death signalling pathways to find new targets for treatment, and using the novel anti-austerity approach to combat the tolerance of cancer cells to nutrient deprivation. Cancers often display high levels of genetic diversity, even within cancers of a particular organ. These genetic differences often make treatments which work with a particular cancer ineffective on another - even from the same origin, and lead to differences in outcomes to selective pressures such as nutrient deprivation. Cur

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35

Latif, Lubna Salah Eldin Abdel. "Assessment of Cell Death Parameters in Bovine Parvovirus-Infected EBTr Cells." BYU ScholarsArchive, 2005. https://scholarsarchive.byu.edu/etd/445.

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Bovine parvovirus (BPV) is a helper-independent parvovirus. It has a small icosahedral capsid with a single stranded DNA genome. It is a highly stable virus with a narrow host range. It causes acute gastroenteritis in calves. It is considered to be a cytolytic virus because it kills the host cells. However, the mechanism by which the virus causes cell death is not known. The work described in this thesis assessed different parameters of cell death in BPV infected embryonic bovine tracheal (EBTr) cells. There are several ways for viruses to induce cell death. Viruses can induce apoptosis in the

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36

Mai, Thi Trang. "Cell death mechanisms of Marmycin A and Salinomycin in cancer cells." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS014.

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Le produit naturel salinomycine (SAL) est largement utilisé comme médicament anticoccidien et maintenant de plus en plus reconnu comme un agent destiné à réduire la proportion de population CD44⁺ / CD24⁻ cellules souches du cancer du sein. Ce facteur est important et intervient lors des rechutes des tumeurs du sein. Pour la première fois, nous avons décrit que l'action n’était pas ionophorique mais que le proton dit "éponge" de la salinomycine ciblait particulièrement la population des cellules souches du cancer. De plus, un analogue alcyne-amine synthétisé de la salinomycine a une action simi

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37

Giampazolias, Evangelos. "Investigating non-apoptotic cell death in cancer." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8056/.

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38

Rijal, Dikchha. "Cell Death Signaling Complexes During Macrophage Differentiation." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36455.

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Monocytes migrate to various tissues and differentiate to macrophages and mediate early control of pathogens. Various alternative pathways of cell death have been discovered which have been shown to play a key role in host survival. Herein, we investigated the impact of differentiation of monocytes to macrophages on their susceptibility to two distinct cell death inducing complexes, ripoptosome and necrosome. Our results indicate that differentiation of macrophages results in resistance to ripoptosome- but not necrosome- induced cell death. Additional experiments indicated that the resistance

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39

O'Hare, Michael J. "Cell cycle related signaling in neuronal death." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/29368.

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Evidence indicates that neuronal loss in the course of neurodegenerative disease often occurs through programmed death processes. The development of effective therapeutic treatments for such diseases requires detailed knowledge of the intracellular signaling pathways controlling these death processes. Previous work has identified cyclin-dependent kinases, a family of kinases normally involved in the control of cell division, as potential regulators of death in neurons. For instance, a number of events that occur during the G1 to S transition in proliferating cells, such as cyclin D/cdk4 activa

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40

Lai, Xin-He. "Francisella tularensis infection induces macrophage cell death." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-295.

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41

Robey, Thomas Edwin. "Reducing fibrosis and cell death in cardiomyoplasty /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8031.

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42

Ménard, Isabelle. "Exploring the many facets of cell death." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111878.

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This thesis summarises research performed with the intent of exploring the many facets of cell death. In the first part of the thesis, the fate of the formin-homology domain containing protein FHOD1 during apoptosis is examined (research performed in the laboratory of Dr. Sophie Roy) and evidence for the cleavage of FHOD1 by caspase-3 at the SVPD616 site is demonstrated. Moreover, the C-terminal FHOD1 cleavage product is shown to translocate to the nucleolus where it inactivates RNA polymerase I transcription.<br>In the second part of the thesis, the role of the RNA-binding protein HuR in canc

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43

Palazzo, Francesco Fausto. "Programmed cell death in autoimmune thyroid disease." Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270709.

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44

Edwards, Susan N. "Regulation of cell death in sympathetic neurons." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316898.

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45

Atkin, Charlotte J. "Developmental cell death in the rat brain." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393568.

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46

Loughery, Jayne Eleanor Patricia. "Mismatch repair, DNA methylation and cell death." Thesis, University of Ulster, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.551565.

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Mismatch repair is a vital DNA repair mechanism whose absence leads to a tolerance towards mutations and a predisposition to colon cancer. MLHl is one of the main proteins involved and is highly conserved from E. coli to human. It not only plays a role in repair, but can signal the cell to die if damage levels become too high. The mechanism by which MLHl triggers cell death in response to damage is not entirely clear, and is likely to differ between normal and cancerous cells. Previous work in the Walsh lab had generated MLH1-depleted subclones of a telomerase- immortalised normal human fibrob

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47

Parnaik, Rahul. "Cell death and clearance in young animals." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284799.

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48

Kreuzaler, Peter Anton. "Cell death modalities in mammary gland involution." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609378.

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49

Wilkinson, Derek. "Proteases and programmed cell death in fungi." Thesis, University of Exeter, 2011. http://hdl.handle.net/10036/3629.

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Programmed cell death in animals, plants and protists is in part regulated by a variety of proteases, including cysteine aspartyl proteases, (caspases, paracaspases and metacaspases), cathepsins, subtilisin-like serine proteases, vacuolar processing enzymes and the proteasome. The role of different proteases in the cell death responses of the fungi is however largely unknown. A greater understanding of the fungal cell death machinery may provide new insights into the mechanisms and evolution of PCD and potentially reveal novel targets for a new generation of antifungal drugs. The role of a met

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50

Dhillon, Harsharan. "Mechanisms of Piperlongumine-Induced Cancer Cell Death." Diss., North Dakota State University, 2015. http://hdl.handle.net/10365/25178.

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Piperlongumine (PPLGM), a bioactive agent obtained from long pepper plants, possesses potent antitumor activity by inducing reactive oxygen species (ROS). However, the mechanisms for PPLGM?s antitumor actions are not well defined. We investigated PPLGM?s antitumor effects and molecular mechanisms against pancreatic and colon cancer, two of the leading causes of cancer death for both men and women in the U.S. We found that PPLGM activated a ROSmediated DNA damage pathway that lead to pancreatic cancer cell death in vitro. Further, mice treated with PPLGM showed reduced pancreatic tumor vo

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