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Dissertations / Theses on the topic 'Endoplasmic reticulum stress'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Johnson, Charlotte. "Targeting endoplasmic reticulum stress and autophagy in cancer." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/84379/.

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Mammalian/mechanistic target of mTOR complex 1 (mTORC1) regulates multiple cellular processes, including de novo protein synthesis, autophagy and apoptosis. mTORC1 overactivation occurs in a range of cancers and benign tumour dispositions as a result of mutations which increase mitogenic stimulus or cause malfunction of the tuberous sclerosis complex, the prime regulator of mTORC1 activity. mTORC1 overactivation results in elevated endoplasmic reticulum (ER) stress which, at low levels, elicits a pro-survival response. However, prolonged or excessive ER stress causes cell death. The present st

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2

Zachariah, Matshediso. "High selenium induces endothelial dysfunction via endoplasmic reticulum stress." Thesis, University of Surrey, 2017. http://epubs.surrey.ac.uk/845246/.

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Selenium (Se) is associated with insulin resistance and may affect endothelial function thereby increasing the risk of type 2 diabetes and associated cardiovascular disease (CVD). However, the molecular mechanisms involved are not clear. The endoplasmic-reticulum (ER) stress response is a mechanism involved in apoptosis induced by high Se in some cancer cells and, also in the pathogenesis of insulin resistance and endothelial dysfunction (ED). Thus, we hypothesised that high Se status causes ED through ER stress response. Endothelial cells (HUVECs) and EA.hy926 cell lines were treated with sel

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3

Voyias, Philip D. "Regulation of endoplasmic reticulum stress in adipose tissue metabolism." Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/74256/.

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Obesity is the most significant risk factor for developing type II diabetes mellitus (T2DM). Obesity induces adipocyte endoplasmic reticulum (ER) stress, prior to onset of insulin resistance. A pathological inability of white adipose tissue (WAT) to expand to accommodate excess energy is predominantly due to impaired adipogenesis. The research hypothesis was that ER stress in human WAT is important in inducing WAT dysfunction and subsequent insulin resistance and T2DM. The aims of this study were to elucidate interactions of ER stress in human WAT and to characterise the role of ER stress in h

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4

Furmanik, Malgorzata. "The role of endoplasmic reticulum stress in vascular calcification." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-endoplasmic-reticulum-stress-in-vascular-calcification(a0138614-e3d8-42ef-9cbf-02a01f6e6eaf).html.

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Vascular calcification (VC) is a health problem common in ageing populations, diabetes and chronic kidney disease. It leads to vascular stiffening and heart failure. VC is a regulated process mediated by vascular smooth muscle cells (VSMCs), with similarities to developmental osteogenesis. The exact molecular events responsible for triggering it are unknown. The endoplasmic reticulum (ER) is involved in folding of proteins. ER stress occurs as a result of unfolded protein accumulation and has been implicated in osteoblast differentiation and bone mineralization. Therefore, I hypothesized that

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5

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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6

Sarkar, Deboleena Dipak. "Potential Role Of Endoplasmic Reticulum Redox Changes In Endoplasmic Reticulum Stress And Impaired Protein Folding In Obesity-Associated Insulin Resistance." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/306999.

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Endoplasmic reticulum (ER) stress plays an important role in the pathogenesis of obesity-related inflammation and insulin resistance in adipose tissue. However, the mechanisms responsible for induction of ER stress are presently unclear. Proper ER redox state is crucial for oxidative protein folding and secretion and impaired protein folding in ER leads to induction of unfolded protein response and ER stress. However, while ER redox state is more oxidizing compared to the rest of the cell, its regulation is poorly understood. In order to determine the effects of ER redox state on development o

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7

Chan, Cheuk-wing Wilson. "ER stress in the pathogenesis of osteochondrodysplasia." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085192.

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8

Preston, Amanda Miriam Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "The role of endoplasmic reticulum stress in beta-cell lipoapoptosis." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41231.

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Beta-cell failure is a key step in the progression from metabolic disorder to overt type 2 diabetes (T2D). This failure is characterised by both secretory defects and loss of beta-cell mass, the latter most likely through increases in the rate of apoptosis. Although the mechanisms underlying these beta-cell defects are unclear, evidence suggests that chronic exposure of beta-cells to elevated fatty acid (FA) plays a role in disease development in genetically susceptible individuals. Furthermore, it has been postulated that endoplasmic reticulum (ER) stress signalling pathways (the unfolded pro

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9

Katsoulieris, Elias. "Oxidatives and Endoplasmic Reticulum Stress in Kidney Priximal Tubule Cells." Thesis, University of Brighton, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506517.

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10

Niederreiter, Lukas. "Endoplasmic reticulum (ER) stress transcription factor Xbp1 in intestinal tumourigenesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708846.

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11

Gaifem, Joana Filipa Madureira. "" Role Of In Endoplasmic Reticulum Stress Response In Sacccharoromyces cerevisiae "." Master's thesis, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/56926.

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12

Bonilla, Myriam. "Endoplasmic reticulum stress linked to calcium signaling in saccharomyces cerevisiae." Available to US Hopkins community, 2003. http://wwwlib.umi.com/dissertations/dlnow/3080627.

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13

Das, Indrajit. "Therapeutic Targeting of Endoplasmic Reticulum Stress in Inflammatory Bowel Disease." Thesis, Griffith University, 2012. http://hdl.handle.net/10072/365999.

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Endoplasmic reticulum (ER) stress occurs when proteins misfold during biosynthesis in the ER. ER stress in intestinal secretory cells has been implicated in the aetiology of inflammatory bowel diseases (IBD) and intestinal inflammation in mice. Intestinal secretory cells are susceptible to ER stress due to high rates of protein synthesis, and ER stress in these cells results in reduced production of cell surface and secreted proteins leading to thinner mucus with a lower anti-microbial content, allowing penetration by luminal microbes, leading to inflammation. Cells experiencing ER stress atte

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14

Gendrisch, Fabian [Verfasser], and Stefan F. [Akademischer Betreuer] Martin. "The role of endoplasmic reticulum stress responses in contact dermatitis." Freiburg : Universität, 2018. http://d-nb.info/1211956318/34.

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15

Martin, Rachel E. "Targeted sensors to monitor oxidative stress in the endoplasmic reticulum." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5884/.

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Hydrogen peroxide has a diverse array of functions in cells. Not only as a mediator of oxidative stress, it is also involved in signalling in many pathways including tyrosine phosphorylation, sumoylation, proliferation and differentiation and cysteine oxidation [1]. There are a number of different producers of hydrogen peroxide in the cell including the NADPH oxidase (Nox) family of enzymes [2], the electron transport chain in the mitochondria [3] and disulfide bond formation in the endoplasmic reticulum (ER) [4]. In order to prevent a toxic build-up of hydrogen peroxide the cell also deploys

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16

Gaifem, Joana Filipa Madureira. "" Role Of In Endoplasmic Reticulum Stress Response In Sacccharoromyces cerevisiae "." Dissertação, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/56926.

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17

Wang, Yongchao. "THE ROLE OF ENDOPLASMIC RETICULUM STRESS IN ETHANOL-INDUCED NEURODEGENERATION." UKnowledge, 2019. https://uknowledge.uky.edu/pharmacol_etds/33.

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Heavy ethanol use causes neurodegeneration manifested by neuronal loss and dysfunction. It is becoming imperative to delineate the underlying mechanism to promote the treatment of ethanol-induced neurodegeneration. Endoplasmic reticulum (ER) stress is a hallmark and an underlying mechanism of many neurodegenerative diseases. This study aims to investigate the role of ER stress in ethanol-induced neurodegeneration. In experimental design, adult mice were exposed to binge ethanol drinking by daily gavage for 1, 5, or 10 days and the response of ER stress was examined. We found the induction of E

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18

Mihai, Adina Daniela. "Obesity-related factors involved in endoplasmic reticulum stress induction in adipocytes." Thesis, Durham University, 2015. http://etheses.dur.ac.uk/11637/.

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Obesity is the most common nutritional disorder in the developed world and represents a major risk factor for associated diseases like type 2 diabetes mellitus, cardiovascular diseases and hypertension. The condition affects the whole body homeostasis but mainly the adipose tissue and is characterised by low grade inflammation, insulin resistance and hyperlipidemia. In adipocytes, it has been associated with endoplasmic reticulum stress (ER stress) induction and activation of the unfolded protein response (UPR). ER stress has been shown to play a central role in the molecular events leading to

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19

Park, Soon Hyang. "The role of endoplasmic reticulum stress signaling in isolated islet apoptosis." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32257.

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A major obstacle to islet transplantation is β-cell death following isolation. Isolation exposes islets to various stresses including endoplasmic reticulum (ER) stress inducers; therefore, the role of ER stress signaling in isolated islet apoptosis was investigated. Activation of eIF2α and JNK1 and XBP1 splicing followed by an increase in caspase-3 activity were observed in isolated human islets. Since the absence of protein-tyrosine phosphatase 1B (PTP1B) was previously shown to reduce ER stress-induced

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20

Hühn, Martin [Verfasser]. "Endoplasmic Reticulum (ER)-stress signalling in the alveolar epithelium / Martin Hühn." Gießen : Universitätsbibliothek, 2013. http://d-nb.info/1065395310/34.

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21

Mahmood, Ahsan. "Role of SLMAP in Endoplasmic Reticulum Stress and Unfolded Protein Response." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24399.

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Cardiac function is regulated by the molecular components of the sarco/endoplasmic reticulum (ER/SR). Disruptions in homeostatic balance of these proteins and calcium regulation results in activation of ER stress response. Sarcolemmal membrane-associated proteins (SLMAPs) are found in cell membrane, SR/ER, and mitochondria. Overexpression of SLMAP in the myocardium has shown to impair excitation-contraction (E-C) coupling in the transgenic (Tg) mice. ER stress response was examined in Tg mice overexpressing SLMAP in the myocardium. In Tg hearts, changes observed in the expression of proteins i

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22

Nakano, Kenzo. "Chloroquine induces apoptosis in pancreatic neuroendocrine neoplasms via endoplasmic reticulum stress." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263541.

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23

Brown, Max Adam. "Investigation of how endoplasmic reticulum stress causes insulin resistance and neuroinflammation." Thesis, Durham University, 2015. http://etheses.dur.ac.uk/11438/.

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Endoplasmic reticulum (ER) stress is caused by the accumulation of mis/unfolded proteins in the ER. ER stress signalling pathways termed the unfolded protein response are employed to alleviate ER stress through increasing the folding capacity and decreasing the folding demand of the ER as well as removing mis/unfolded proteins. However, ER stress signalling pathways induce diverse cellular changes beyond changes to the ER. This study aims to further investigate some of these ER stress-mediated events. ER stress can cause activation of JNK. Prolonged ER stress-mediated JNK activation is reporte

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24

Fonseca, Sonya G. "Role of WFS1 in Regulating Endoplasmic Reticulum Stress Signaling: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/414.

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The endoplasmic reticulum (ER) is a multi-functional cellular compartment that functions in protein folding, lipid biosynthesis, and calcium homeostasis. Perturbations to ER function lead to the dysregulation of ER homeostasis, causing the accumulation of unfolded and misfolded proteins in the cell. This is a state of ER stress. ER stress elicits a cytoprotective, adaptive signaling cascade to mitigate stress, the Unfolded Protein Response (UPR). As long as the UPR can moderate stress, cells can produce the proper amount of proteins and maintain a state of homeostasis. If the UPR, however, is

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25

Shank, Karin Janel. "Coordination of the endoplasmic reticulum stress response and lipid metabolism in plants." NCSU, 2000. http://www.lib.ncsu.edu/theses/available/etd-20000729-161702.

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<p>The endoplasmic reticulum (ER) stress response is an important signal transduction pathway that senses ER stress caused by misfolded proteins or increased secretory protein traffic and induces molecular chaperone expression to counter such stress. The response has been well characterized in yeast and mammals where it has been associated with a variety of metabolic pathways, such as phospholipid biosynthesis, translational inhibition, and ER associated degradation. In plants, however, the connections of the ER stress response with metabolic pathways other than those involved in chaperone bio

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26

Misiewicz, Michael. "Identification of a novel endoplasmic reticulum stress response element regulated by XBP1." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116963.

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The Prion protein (PrP), which is the causative agent of scrapie diseases, has a still unclear physiological function, despite 30 years of research on its nature. However, a preponderance of evidence is beginning to support the idea that cellular prion protein (PrPC) has a pro-survival function. Here, we study the regulation of the prion protein gene (PRNP) in this context, as the regulation of the PRNP gene is not well understood. By homology, we identified in the PRNP a novel promoter element which bears similarity to the Endoplasmic Reticulum Stress Response Element (ERSE). This novel ERSE

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27

Lari, Federica. "Resolution of proteotoxic stress in the endoplasmic reticulum by ubiquitin ligase complexes." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:871e0484-3de4-4d0d-8206-4af16a8b743e.

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The eukaryotic endoplasmic reticulum (ER) is a multifunctional organelle, primarily responsible for the folding and maturation of secretory proteins, as well as lipid metabolism, calcium homeostasis, ubiquitin-dependent signalling and cell fate decisions. ER-associated degradation (ERAD) oversees protein folding and delivers misfolded proteins for degradation by the proteasome via ubiquitin conjugation mediated by RING-type E3 ubiquitin ligases. An intact ERAD is crucial to cellular homeostasis, as unresolved protein imbalances cause ER stress that ultimately lead to apoptosis. The human ER ac

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28

Levet, Clémence. "Mild Endoplasmic Reticulum Stress Protects From Cell Death : The Role Of Autophagy." Thesis, Lyon 1, 2012. http://www.theses.fr/2012LYO10209.

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Ces dernières années ont été très fructueuses pour l'identification des mécanismes fondamentaux de l'apoptose chez les métazoaires. Cependant, il reste beaucoup à apprendre sur la manière dont sont régulés les programmes de mort en fonction du type cellulaire. Un excès d'apoptose des neurones peut conduire à différentes pathologies neurodégénératives comme les maladies de Huntington, Parkinson ou Alzheimer. La neurodégénérescence est souvent associée à un stress du réticulum endoplasmique (RE), à l'autophagie et à un stress oxydatif. Cependant le rôle de ces mécanismes dans la régulation de la

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Page, Lindsay N. "Endoplasmic Reticulum Stress Contributes to Cyclosporine A-Induced Lens Epithelial Cell Loss." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1585948655611948.

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30

Bicknell, Alicia Anne. "Two MAP kinases regulate novel aspects of the endoplasmic reticulum stress response." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3369545.

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Thesis (Ph. D.)--University of California, San Diego, 2009.<br>Title from first page of PDF file (viewed September 14, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 160-185).

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31

Pino, Steven C. "Role of Endoplasmic Reticulum Stress Response Signaling in T Cells: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/381.

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T cells play a central role in cellular-mediated immunity and must become activated to participate as effector cells in the immune response. The activation process is highly intricate and involves stimulation of a number of downstream signaling pathways enabling T cells to proliferate and produce cytokines that are vital for proper effector function. This increase in protein production and protein folding activity adds to the normal physiological strain on cellular machinery. One cellular compartment that has generated a mechanism to mitigate the stress induced by increased protein production

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32

Thomas, Sally Edwina. "The role of cell cycle checkpoints in the survival of endoplasmic reticulum stress." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608043.

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33

Tan, Zhijia, and 谭志佳. "Molecular analyses of chondrocyte differentiation and adaptation to ER stress." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/209435.

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Endochondral bone development depends on the progression of chondrocyte proliferation, hypertrophy and terminal differentiation, which requires precise transcriptional regulation and signaling coordination. Disturbance of this process would disrupt chondrocyte differentiation and lead to chondrodysplasias. In cells, a highly conserved mechanism, ER stress signaling, has been developed to sense the protein load and maintain the cellular homeostasis. In humans, mutations in COL10A1 induce ER stress and result in metaphyseal chondrodysplasia type Schmid (MCDS). Previous analysis of a MCDS mouse m

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34

Gwiazda, Kamila Sabina. "Role of endoplasmic reticulum calcium stores in beta-cell ER stress and lipotoxicity." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/12553.

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There are strong links between obesity, elevated free fatty acids, and type 2 diabetes. Specifically, the saturated fatty acid palmitate has pleiotropic effects on β-cell function and survival. The present study sought to determine the mechanism by which palmitate affects intracellular Ca²⁺ in pancreatic β-cells, and in particular the role of the endoplasmic reticulum (ER). In the MIN6 β-cell line, palmitate rapidly increased cytosolic Ca²⁺ through a combination of Ca²⁺ store release and extracellular Ca²⁺ influx. Palmitate caused a reversible lowering of ER Ca²⁺, measured directly with the fl

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35

Tillman, Erik J. (Erik James). "Genetic analysis of endoplasmic reticulum homeostasis during stress and infection of Caenorhabditis elegans." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/119917.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2018.<br>This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.<br>Cataloged from student-submitted PDF version of thesis.<br>Includes bibliographical references.<br>Animals experience intrinsic and extrinsic stressors throughout development and adulthood. To maintain cellular and organismal homeostasis, eukaryota and metazoa rely on conserved, integrated stress response pathways. Throughout its life cycle, the free-living nem

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36

Nugent, Ashleigh Elizabeth. "The Presence of Extracellular Matrix Alters the Chondrocyte Response to Endoplasmic Reticulum Stress." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1271375344.

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37

Mlynarczyk, Coraline. "Regulation of p21CDKN1A in the endoplasmic reticulum stress response : mechanism, function and implications." Paris 7, 2013. http://www.theses.fr/2013PA077128.

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Dans les tumeurs solides, un apport réduit en nutriments et oxygène génère un stress au niveau du réticulum endoplasmique (RE). Nous avons précédemment montré que la réponse physiologique déclenchée (UPR) induit p53/47, une protéine isoforme de p53. P53/47 provoque un arrêt du cycle cellulaire en G2, via 14-3-3 sigma, pour rétablir l'homéostasie du RE. Ceci contraste avec le blocage en Gl par p21 qui est activé par p53 suite à un dommage de F ADN. La majorité des traitements contre le cancer étant basée sur l'utilisation d'agents génotoxiques, nous avons cherché à comprendre comment un stress

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38

Zha, Beth Shoshana. "HIV Protease Inhibitors Trigger Lipid Metabolism Dysregulation Through Endoplasmic Reticulum Stress and Autophagy." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/273.

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HIV protease inhibitors (PI) are core components of Highly Active Antiretroviral Therapy (HAART). HIV PIs are extremely effective at suppressing viral load, but have been linked to lipodystrophy and dyslipidemia, which are major risk factors for cardiovascular disease. Recent studies indicate that activation of endoplasmic reticulum (ER) stress is an important cellular mechanism underlying HIV PI-induced dysregulation of lipid metabolism. However, the exact role of ER stress in HIV PI-associated lipodystrophy and dyslipidemia remains to be identified. Hepatocytes and adipocytes are important p

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39

Egawa, Naohiro. "The endoplasmic reticulum stress sensor, ATF6α, protects against neurotoxin-induced dopaminergic neuronal death". Kyoto University, 2011. http://hdl.handle.net/2433/142092.

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Lipson, Kathryn L. "The Role of Endoplasmic Reticulum Stress Signaling in Pancreatic Beta Cells: a Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/363.

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Protein folding in the endoplasmic reticulum (ER) is essential for proper cellular function. However, the sensitive environment in the ER can be perturbed by both pathological processes as well as by physiological processes such as a large biosynthetic load placed on the ER. ER stress is a specific type of intracellular stress caused by the accumulation of immature or abnormal misfolded or unfolded proteins in the ER. Simply defined, ER stress is a disequilibrium between ER load and folding capacity. Cells have an adaptive response that counteracts ER stress called the "Unfolded Protein Respon

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Herrenbruck, Adrienne Rose. "EFFECTS OF HIGH FAT EXPOSURE ON SKELETAL MUSCLE AUTOPHAGY AND ENDOPLASMIC RETICULUM STRESS." UKnowledge, 2018. https://uknowledge.uky.edu/khp_etds/53.

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Autophagy is a major degradation mechanism, responsible for clearing damaged and dysfunctional organelles, including the endoplasmic reticulum, a structure essential for protein synthesis and myocellular hypertrophy. Alterations in autophagy throughout various tissues of the body have been linked to various negative side effects such as decreased myocellular hypertrophy and insulin resistance. High fat diets lead to changes (both increases and decreases) in autophagy in various tissues throughout the body in a tissue-specific manner. Skeletal muscle autophagy is decreased in myotubes cultured

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Pirot, Pierre. "Identification and characterization of the endoplasmic reticulum (ER)-stress pathways in pancreatic beta-cells." Doctoral thesis, Universite Libre de Bruxelles, 2007. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210623.

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The endoplasmic reticulum (ER) is the organelle responsible for synthesis and folding of secreted and membranous protein and lipid biosynthesis. It also functions as one of the main cellular calcium stores. Pancreatic beta-cells evolved to produce and secrete insulin upon demand in order to regulate blood glucose homeostasis. In response to increases in serum glucose, insulin synthesis represents nearly 50% of the total protein biosynthesis by beta-cells. This poses an enormous burden on the ER, rendering beta-cells vulnerable to agents that perturb ER function. Alterations of ER homeostasis l

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Al-Sheikh, Hashem M. "Transcriptional regulation of the glucoamylase-encoding gene under endoplasmic reticulum stress in Aspergillus niger." Thesis, University of Nottingham, 2005. http://eprints.nottingham.ac.uk/13097/.

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The ability of many filamentous fungi, such as Aspergillus niger, to secret a high level of homologous proteins has led to their consideration as hosts for the production of heterologous proteins. However, the levels of some secreted heterologous proteins have often been low. Although many strategies have been developed to improve the level of secreted heterologous proteins, further studies into the remaining bottlenecks are required. One common strategy used to improve secreted protein production from filamentous fungi is to express the target protein under the control of a highly-induced nat

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Carne, Naomi Angharad. "The effect of endoplasmic reticulum and reductive stress on the human dermal fibroblast proteome." Thesis, Durham University, 2018. http://etheses.dur.ac.uk/12794/.

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Dermal fibroblasts are responsible for the secretion of extracellular matrix (ECM) components that support the structural integrity of the skin. Alterations to the ECM have been implicated in many skin diseases including systemic sclerosis and fibrotic disorders, as well as wrinkle formation and wound healing in the aged phenotype. The endoplasmic reticulum (ER) is responsible for the production and quality control of secreted proteins, and perturbations to its correct function could therefore lead to aberrant ECM deposition from dermal fibroblasts. ER stress occurs when homeostasis of this or

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45

Coelho, Dina Raquel da Silva. "The Role of the Endoplasmic Reticulum Stress Transducer Ire1 during Photoreceptor Differentiation in Drosophila." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2013. http://hdl.handle.net/10362/12071.

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Dissertation presented to obtain the Ph.D degree in Biology.<br>The accumulation of misfolded proteins in the lumen of the endoplasmic reticulum (ER) causes ER stress and activates a homeostatic mechanism termed the Unfolded Protein Response (UPR). The most conserved arm of the UPR is mediated by the ER transmembrane protein Ire1 that removes an unconventional intron from Xbp1 mRNA upon ER stress. Xbp1spliced is an effective transcription factor that up-regulates ER chaperones and enzymes.(...)

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46

Hata, Masayuki. "KUS121, a VCP modulator, attenuates ischemic retinal cell death via suppressing endoplasmic reticulum stress." Kyoto University, 2018. http://hdl.handle.net/2433/232075.

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47

Li, Yi. "Mechanisms of Transcriptional Regulation of Cat-1 Gene Expression by Endoplasmic Reticulum (ER) Stress." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1238790728.

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48

DuRose, Jenny Bratlien. "The unfolded protein response integrating stress signals from the endoplasmic reticulum to the nucleolus /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3330123.

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Thesis (Ph. D.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed November 13, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.

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49

López, Ignacio. "P53-mediated control of mRNA translation during Endoplasmic Reticulum stress : mechanisms and physiological implications." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC220/document.

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Des fluctuations physiologiques lors de la production et du repliement des protéines, ainsi que des processus pathologiques comme l’infection virale, le vieillissement et les cancers peuvent conduire à un stress du Réticulum Endoplasmique (RE). Il s’agit d’un état caractérisé par l’accumulation de protéines non/mal repliées dans la lumière du RE, qui déclenche la réponse aux protéines dépliées, dite UPR (Unfolded Protein Response). Pour rétablir l’équilibre protéique, la réponse UPR va inhiber la synthèse protéique globale cap-dépendante et favoriser la production de protéases et de chaperonne

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Yang, Ling. "Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes." Kent State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=kent1175103480.

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