subject:(Endoplasmic reticulum stress)

University of Cambridge

1. Capatina, Nadejda. Role of Endoplasmic Reticulum Stress in Trophoblast Stem Cell Differentiation.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/298767

► The project aimed to provide a mechanistic understanding of the effect of endoplasmic reticulum (ER) stress on the differentiation of trophoblast stem cells (TSCs), placental… (more)

Subjects/Keywords: endoplasmic reticulum stress; trophoblast; stem cell differentiation

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APA (6^th Edition):

Capatina, N. (2019). Role of Endoplasmic Reticulum Stress in Trophoblast Stem Cell Differentiation. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/298767

Chicago Manual of Style (16^th Edition):

Capatina, Nadejda. “Role of Endoplasmic Reticulum Stress in Trophoblast Stem Cell Differentiation.” 2019. Doctoral Dissertation, University of Cambridge. Accessed April 21, 2021. https://www.repository.cam.ac.uk/handle/1810/298767.

MLA Handbook (7^th Edition):

Capatina, Nadejda. “Role of Endoplasmic Reticulum Stress in Trophoblast Stem Cell Differentiation.” 2019. Web. 21 Apr 2021.

Vancouver:

Capatina N. Role of Endoplasmic Reticulum Stress in Trophoblast Stem Cell Differentiation. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Apr 21]. Available from: https://www.repository.cam.ac.uk/handle/1810/298767.

Council of Science Editors:

Capatina N. Role of Endoplasmic Reticulum Stress in Trophoblast Stem Cell Differentiation. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/298767

Université de Bordeaux I

2. Bouchecareilh, Marion. Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer.

Degree: Docteur es, Biologie cellulaire et physiopathologie, 2008, Université de Bordeaux I

URL: http://www.theses.fr/2008BOR13711

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Le Réticulum endoplasmique (RE) est le premier compartiment intracellulaire traversé par les protéines sécrétées. Au sein de cet organite, les protéines acquièrent une conformation native,… (more)

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Le Réticulum endoplasmique (RE) est le premier compartiment intracellulaire traversé par les protéines sécrétées. Au sein de cet organite, les protéines acquièrent une conformation native, et subissent de nombreuses modifications post-traductionnelles telles que la N-glycosylation ou la formation de ponts disulfures. Dans certaines conditions (stress réducteurs, hypoxie, privation en glucose…) des protéines anormalement conformées s’accumulent au sein du RE ce qui conduit à l’induction de l'Unfolded Protein Response (UPR). Cette réponse va alors tout d’abord induire l’inhibition de la traduction, ce qui limite l’entrée de nouvelles protéines dans le RE. En parallèle, un programme transcriptionnel spécifique conduit à l’augmentation de l’expression de protéines impliquées dans le repliement et la dégradation des protéines accumulées dans la lumière du RE. Cette réponse adaptative intégrée est contrôlée principalement par 3 protéines transmembranaires du RE : PERK (PKR-related ER kinase), ATF6 (Activating transcription factor) et enfin IRE1 (Inositol requiring kinase 1) sur laquelle porte notre étude. Au cours de ma thèse, j’ai tout d’abord participé à une étude démontrant que l’activation des voies de signalisation dépendantes d’IRE1 contribuait à la surexpression du VEGF-A in vitro et régulait l’angiogenèse et la croissance tumorale in vivo dans un modèle de greffe orthotopique de cellules U87 dérivées de gliomes humains. Cette protéine pourrait donc constituer une cible thérapeutique potentielle. Ces résultats nous ont par conséquent amenés à identifier des modulateurs de l’activité de la protéine IRE1. Pour cela nous avons développé un test in vitro permettant d’évaluer l’étape essentielle dans l’activation de la protéine IRE1, sa dimérisation. Ce test nous a permis d’identifier un peptide capable d’interférer dans la formation des dimères de la protéine IRE1, mais aussi et de façon inattendue, d’accroître son activité endoribonucléase in vitro et in vivo. Ainsi, nous proposons que ce peptide interfacial issu du domaine kinase de la protéine IRE1 pourrait promouvoir un changement conformationnel du domaine cytosolique de la protéine entière et par conséquent, potentialiserait de façon significative son activité endoribonucléasique. Ce modulateur identifié pourrait donc représenter un nouvel outil à potentiel thérapeutique utilisable par exemple dans des maladies conformationnelles.

The endoplasmic Reticulum (ER) is the first intracellular compartment encountered by secretory proteins. In this organelle proteins acquire their correct conformation and undergo many post-translational modifications such as N-glycosylation or disulphide bond formation. Under specific environmental conditions (reductive stress, hypoxia, glucose deprivation …), protein folding is perturbed and uncorrectly folded proteins accumulate in the lumen of the ER. This leads to the activation of an adaptive response named the Unfolded Protein Response (UPR). The UPR consists in an attenuation of protein translation and an activation of a…

Advisors/Committee Members: Moenner, Michel (thesis director), Chevet, Eric (thesis director).

Subjects/Keywords: Réticulum Endoplasmique; Stress; Cancer; Ire1; Endoplasmic Reticulum; Stress; Cancer; Ire1

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APA (6^th Edition):

Bouchecareilh, M. (2008). Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer. (Doctoral Dissertation). Université de Bordeaux I. Retrieved from http://www.theses.fr/2008BOR13711

Chicago Manual of Style (16^th Edition):

Bouchecareilh, Marion. “Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer.” 2008. Doctoral Dissertation, Université de Bordeaux I. Accessed April 21, 2021. http://www.theses.fr/2008BOR13711.

MLA Handbook (7^th Edition):

Bouchecareilh, Marion. “Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer.” 2008. Web. 21 Apr 2021.

Vancouver:

Bouchecareilh M. Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer. [Internet] [Doctoral dissertation]. Université de Bordeaux I; 2008. [cited 2021 Apr 21]. Available from: http://www.theses.fr/2008BOR13711.

Council of Science Editors:

Bouchecareilh M. Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer. [Doctoral Dissertation]. Université de Bordeaux I; 2008. Available from: http://www.theses.fr/2008BOR13711

Colorado State University

3. Estrada, Andrea Lee. Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The.

Degree: PhD, Food Science and Human Nutrition, 2017, Colorado State University

URL: http://hdl.handle.net/10217/185714

► Non-alcoholic fatty liver disease (NAFLD) is currently a significant health concern in both adults and children. NAFLD is a disease characterized by accumulation of fat… (more)

▼ Non-alcoholic fatty liver disease (NAFLD) is currently a significant health concern in both adults and children. NAFLD is a disease characterized by accumulation of fat in the liver (steatosis) in the absence of chronic alcohol consumption. In some individuals, steatosis progresses to non-alcoholic steatohepatitis (NASH), which is characterized by steatosis, inflammation, apoptosis and fibrosis, and can ultimately lead to end-stage liver disease. The underlying causes of NAFLD are unclear, although recent evidence has implicated the endoplasmic reticulum (ER) in both the development of steatosis and progression to NASH. Disruption of ER homeostasis or "ER stress" has been observed in the livers and adipose tissue of humans with NAFLD and/or obesity. Downstream signaling events that arise from ER stress include lipid biogenesis, insulin resistance, inflammation, fibrosis and apoptosis, all of which are hallmark features of NAFLD and NASH. Elevated circulating free fatty acids are a characteristic feature of humans with NAFLD and are positively correlated with disease severity. Our laboratory has demonstrated that in rodents, selective elevation of circulating free fatty acids induces ER stress in liver and adipose tissue. In addition, ER stress is exacerbated when the composition of fatty acids includes levels of saturated fats comparable to what is encountered in the typical western diet. We, and others, have also demonstrated that saturated fatty acids provoke ER stress in cultured hepatocytes, pancreatic beta cells, and various other cell types. These data have led to the hypothesis that the composition of fatty acids presented to and stored within the liver is an important determinant of ER homeostasis. ER stress is characterized by an accumulation of unfolded proteins within the lumen of the ER. Therefore, the presence of ER stress in NAFLD implies that there is an imbalance between the protein load presented to the ER, and the ability of the ER to process, degrade and/or remove these proteins. The overall aim of this thesis was to examine how saturated fatty acids disrupt ER homeostasis in the liver. We explored in vivo hepatic protein synthesis in response to acute dietary intervention, namely using diets high saturated fat and sucrose, which promote hepatic steatosis and insulin resistance in rats. We utilized the saturated fat, palmitate in controlled delivery to H4IIE liver hepatocytes in order to assess protein synthesis and components of protein degradation. Lastly, we examined the roles of calcium homeostasis and protein palmitoylation in response to palmitate treatment in H4IIE liver hepatocytes. We found that diets high in saturated fat did not affect hepatic protein synthesis in rats. In agreement with this observation, H4IIE hepatocyte treatment with palmitate did not selectively stimulate cellular protein synthesis. Provision of palmitate increased protein ubiquitination, this result was observed independent of proteasome activity or total cellular protein degradation. Lastly, we found that… Advisors/Committee Members: Pagliassotti, Michael (advisor), Miller, Benjamin (committee member), Foster, Michelle (committee member), Frye, Melinda (committee member), Gentile, Christopher (committee member).

Subjects/Keywords: endoplasmic reticulum stress; protein synthesis; saturated fatty acids; non-alcoholic fatty liver disease; endoplasmic reticulum; proteostasis

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APA (6^th Edition):

Estrada, A. L. (2017). Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/185714

Chicago Manual of Style (16^th Edition):

Estrada, Andrea Lee. “Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The.” 2017. Doctoral Dissertation, Colorado State University. Accessed April 21, 2021. http://hdl.handle.net/10217/185714.

MLA Handbook (7^th Edition):

Estrada, Andrea Lee. “Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The.” 2017. Web. 21 Apr 2021.

Vancouver:

Estrada AL. Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The. [Internet] [Doctoral dissertation]. Colorado State University; 2017. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10217/185714.

Council of Science Editors:

Estrada AL. Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The. [Doctoral Dissertation]. Colorado State University; 2017. Available from: http://hdl.handle.net/10217/185714

University of Otago

4. Seo, Benedict Lloyd. Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model .

Degree: 2011, University of Otago

URL: http://hdl.handle.net/10523/2041

► The endoplasmic reticulum (ER) is an organelle of great importance. It represents the intracellular site for protein synthesis, folding, and post-translational modification. Intricately related processes… (more)

▼ The endoplasmic reticulum (ER) is an organelle of great importance. It represents the intracellular site for protein synthesis, folding, and post-translational modification. Intricately related processes that oversee the proper folding of newly synthesized polypeptides, secretion of native proteins and degradation of those species that have failed to achieve correct conformations for export, collectively govern the homeostasis of the ER. ER stress reflects the state where there is an imbalance between the influx of polypeptides and the net efflux of proteins from the ER. This may result from an increase in the demand for protein synthesis and resulting cellular indigestion. Accumulation of mutated or unfolded proteins may also cause this phenomenon. The human unfolded protein response (UPR) is induced by ER stress. The UPR comprises three pathways that initiate mechanisms to overcome the ER stress. Upon detection of stress stimuli, various molecular chaperones and folding enzymes are induced to facilitate and accelerate protein folding. At the same time, global translational attenuation may result in decreasing the protein load into the ER. Some pathways also activate transcriptional factors to up-regulate genes involved in the endoplasmic reticulum quality control (ERQC) and endoplasmic reticulum associated degradation (ERAD) processes. Ultimately, the cell may recover from stress, or apoptosis may be induced where the stress is irrevocable. Russell bodies (RB) are round eosinophilic intracellular structures that represent distended ER cisternae. They are composed of mutated immunoglobulins, and are commonly observed associated with plasma cells. RBs have been documented in neurodegenerative diseases, chronic inflammatory diseases, as well as in lymphoproliferative conditions. The accumulation of transport-incompetent proteins in the ER has been theorized as the usual cause for this morphological phenomenon. To that end, it had been suggested that RBs originate as a SOS compartment, where abnormal proteins, which cannot be secreted, but have escaped intracellular degradation, can be accumulated without blocking the normal secretory pathway. However, to date, it is not clear precisely which part of the UPR processes are involved in this phenomenon leading to the biogenesis of RB. In order to elucidate the relationship between inflamed tissues containing RB and ER stress, three hypotheses were addressed in this research; firstly, that ‘RB will be present in association with periodontal inflammation’, secondly that ‘the pattern of GRP-78 expression will differ based on the presence of RB’, and finally, that ‘gene expression patterns of UPR will differ based on the presence of RB’. To address these hypotheses, chronically inflamed human periodontal tissues were used to identify and quantify RB. RB were identified microscopically and quantified in terms of RB per 1mm2 of a specimen. Histochemical techniques known to stain RB (Haematoxylin and eosin (H&E), periodic-acid Schiff (PAS), and methyl green pyronin… Advisors/Committee Members: Rich, Alison (advisor).

Subjects/Keywords: Endoplasmic reticulum stress; Russell Bodies; Unfolded protein response

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Seo, B. L. (2011). Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/2041

Chicago Manual of Style (16^th Edition):

Seo, Benedict Lloyd. “Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model .” 2011. Doctoral Dissertation, University of Otago. Accessed April 21, 2021. http://hdl.handle.net/10523/2041.

MLA Handbook (7^th Edition):

Seo, Benedict Lloyd. “Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model .” 2011. Web. 21 Apr 2021.

Vancouver:

Seo BL. Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model . [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10523/2041.

Council of Science Editors:

Seo BL. Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model . [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/2041

Universiteit Utrecht

5. Renne, M.F. Endoplasmic Reticulum Stress and lipid metabolism.

Degree: 2014, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/296878

► Upon endoplasmic reticulum (ER) stress, the unfolded protein response (UPR) triggers cellular mechanisms to restore ER homeostasis. Aberrancies in lipid homeostasis can cause alterations in… (more)

Subjects/Keywords: Unfolded protein response; lipid metabolism; endoplasmic reticulum stress; membrane fluidity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Renne, M. F. (2014). Endoplasmic Reticulum Stress and lipid metabolism. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/296878

Chicago Manual of Style (16^th Edition):

Renne, M F. “Endoplasmic Reticulum Stress and lipid metabolism.” 2014. Masters Thesis, Universiteit Utrecht. Accessed April 21, 2021. http://dspace.library.uu.nl:8080/handle/1874/296878.

MLA Handbook (7^th Edition):

Renne, M F. “Endoplasmic Reticulum Stress and lipid metabolism.” 2014. Web. 21 Apr 2021.

Vancouver:

Renne MF. Endoplasmic Reticulum Stress and lipid metabolism. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2021 Apr 21]. Available from: http://dspace.library.uu.nl:8080/handle/1874/296878.

Council of Science Editors:

Renne MF. Endoplasmic Reticulum Stress and lipid metabolism. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/296878

University of Rochester

6. Syc-Mazurek, Stephanie B. The Molecular Signaling Pathways Controlling Apoptotic Retinal Ganglion Cell Death after Axonal Injury.

Degree: PhD, 2017, University of Rochester

URL: http://hdl.handle.net/1802/32918

► Vision loss in glaucoma is characterized by the stereotypical death of retinal ganglion cells (RGCs). Ocular hypertension is a major risk factor for glaucoma and… (more)

▼ Vision loss in glaucoma is characterized by the stereotypical death of retinal ganglion cells (RGCs). Ocular hypertension is a major risk factor for glaucoma and is thought to trigger glaucomatous neurodegeneration through injury to RGC axons. The cellular signaling pathway leading from ocular hypertension to RGC degeneration, however, is not well defined. Understanding the molecular pathways that contribute to glaucomatous neurodegeneration will inform the rational design of new pharmacologic interventions. The focus of these studies was to identify the molecular signaling pathway(s) critical for RGC death in glaucoma. JNK-JUN signaling, a component of the mitogen-activated protein kinase (MAPK) family, is a regulator of neurodegeneration in many different systems. After mechanical axon injury, an injury thought to mimic glaucomatous damage to RGC axons, JNK-JUN signaling has been shown to be important in RGC death. To determine if JNK-JUN signaling is active in RGCs after an ocular hypertensive insult, the expression of JUN and JNK were tested in the DBA/2J mouse, a mouse model of ocular hypertension. JUN and JNK were found to be activated in a temporal and spatial pattern consistent with regulating glaucomatous neurodegeneration. To assess the importance of this pathway after an ocular hypertensive injury, optic nerves from Jun deficient and wild type aged DBA/2J mice were scored for optic nerve damage. No difference was observed in the severity of optic nerve damage between genotypes, with both groups having significant axonal degeneration. Jun deficiency did significantly protect RGC bodies (somas) as compared to control eyes. Despite the protection to RGC somas conferred by Jun deficiency after ocular hypertensive injury, Jun deficiency did not provide complete protection to RGC somas. Furthermore, after mechanical optic nerve crush Jun deficiency did not protect all RGCs at extended time points after injury. Together these data suggest another pro-death signaling pathway is critical for RGC somal degeneration after axonal injury. Another major regulator of axon injury induced RGC death is endoplasmic reticulum (ER) stress, specifically its target gene, Ddit3. JUN and DDIT3 expression were found to be independently regulated in RGCs after axonal injury, suggesting each can independently control axonal injury induced RGC death. To test the possibility that JUN and DDIT3 together control RGC fate after injury, Jun and Ddit3 deficient mice were generated and subjected to optic nerve injury. Inhibiting these two pathways together appears to have an additive effect on RGC survival, providing profound/near complete protection even at extended time points after optic nerve crush. These results suggest JUN and DDIT3 are independently regulated pro-death signaling molecules in RGCs and together control apoptotic signaling in RGCs after axonal injury. Preventing glaucomatous neurodegeneration will likely require the inhibition of several pro-death signaling pathways as both MAPK and ER…

Subjects/Keywords: Axonopathy; Endoplasmic reticulum stress; Glaucoma; Mitogen activated kinase signaling; Neurodegeneration

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Syc-Mazurek, S. B. (2017). The Molecular Signaling Pathways Controlling Apoptotic Retinal Ganglion Cell Death after Axonal Injury. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/32918

Chicago Manual of Style (16^th Edition):

Syc-Mazurek, Stephanie B. “The Molecular Signaling Pathways Controlling Apoptotic Retinal Ganglion Cell Death after Axonal Injury.” 2017. Doctoral Dissertation, University of Rochester. Accessed April 21, 2021. http://hdl.handle.net/1802/32918.

MLA Handbook (7^th Edition):

Syc-Mazurek, Stephanie B. “The Molecular Signaling Pathways Controlling Apoptotic Retinal Ganglion Cell Death after Axonal Injury.” 2017. Web. 21 Apr 2021.

Vancouver:

Syc-Mazurek SB. The Molecular Signaling Pathways Controlling Apoptotic Retinal Ganglion Cell Death after Axonal Injury. [Internet] [Doctoral dissertation]. University of Rochester; 2017. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/1802/32918.

Council of Science Editors:

Syc-Mazurek SB. The Molecular Signaling Pathways Controlling Apoptotic Retinal Ganglion Cell Death after Axonal Injury. [Doctoral Dissertation]. University of Rochester; 2017. Available from: http://hdl.handle.net/1802/32918

University of Alberta

7. Lara, Carlos J. The Herp and HRD1-dependent degradation of TRPP2.

Degree: MS, Department of Physiology, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/p8418n98g

► Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a prevalent genetic disorder where multiple fluid-filled cysts destroy kidney architecture, eventually requiring hemodialysis or kidney transplant. Approximately… (more)

Subjects/Keywords: calcium signaling; endoplasmic reticulum stress; polycystic kidney disease; Herp; HRD1; TRPP2

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APA (6^th Edition):

Lara, C. J. (2012). The Herp and HRD1-dependent degradation of TRPP2. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/p8418n98g

Chicago Manual of Style (16^th Edition):

Lara, Carlos J. “The Herp and HRD1-dependent degradation of TRPP2.” 2012. Masters Thesis, University of Alberta. Accessed April 21, 2021. https://era.library.ualberta.ca/files/p8418n98g.

MLA Handbook (7^th Edition):

Lara, Carlos J. “The Herp and HRD1-dependent degradation of TRPP2.” 2012. Web. 21 Apr 2021.

Vancouver:

Lara CJ. The Herp and HRD1-dependent degradation of TRPP2. [Internet] [Masters thesis]. University of Alberta; 2012. [cited 2021 Apr 21]. Available from: https://era.library.ualberta.ca/files/p8418n98g.

Council of Science Editors:

Lara CJ. The Herp and HRD1-dependent degradation of TRPP2. [Masters Thesis]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/p8418n98g

University of Alberta

8. Deslauriers, Andre. Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger.

Degree: MS, Department of Medical Microbiology and Immunology, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/bg257g06z

► Endoplasmic reticulum (ER) stress is a homeostatic mechanism, which is utilized by cells to adapt to inter- and intra-cellular changes. There is a burgeoning literature… (more)

Subjects/Keywords: Human Endougenous Retroviruses; Endoplasmic Reticulum Stress; Multiple Sclerosis

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APA (6^th Edition):

Deslauriers, A. (2010). Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/bg257g06z

Chicago Manual of Style (16^th Edition):

Deslauriers, Andre. “Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger.” 2010. Masters Thesis, University of Alberta. Accessed April 21, 2021. https://era.library.ualberta.ca/files/bg257g06z.

MLA Handbook (7^th Edition):

Deslauriers, Andre. “Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger.” 2010. Web. 21 Apr 2021.

Vancouver:

Deslauriers A. Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger. [Internet] [Masters thesis]. University of Alberta; 2010. [cited 2021 Apr 21]. Available from: https://era.library.ualberta.ca/files/bg257g06z.

Council of Science Editors:

Deslauriers A. Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger. [Masters Thesis]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/bg257g06z

9. Rafiei, Hossein 1981-. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.

Degree: 2017, University of Saskatchewan

URL: http://hdl.handle.net/10388/7946

► Non-alcoholic fatty liver disease (NAFLD) is a public health burden. Steatosis as the “first hit”, and oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress… (more)

▼ Non-alcoholic fatty liver disease (NAFLD) is a public health burden. Steatosis as the “first hit”, and oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress as the “second hits” are the main contributors of the progression of fatty liver to non-alcoholic steatohepatitis (NASH). Dietary polyphenols have shown promise in protecting the liver against NAFLD. The relative effectiveness and mechanisms of different polyphenols however is mostly unknown. In this thesis HepG2 hepatocytes exposed to oleic or palmitic acid were used as a model system to explore the ability of selected polyphenols (resveratrol, quercetin, catechin, cyanidin, cyanidin-3-glucoside, berberine) from different classes to protect against molecular aspects of NAFLD and NASH. In an investigation of the “first hit” (Chapter 3), different polyphenols protected similarly against oleic acid-induced intracellular lipid accumulation, but differed in their effects on the expression of genes and proteins involved in lipogenesis, fatty acid oxidation, mitochondrial biogenesis, and bioenergetics. In an investigation of “second hits” (Chapter 4), most of the polyphenols decreased reactive oxygen species (ROS), prevented the decrease in uncoupling protein 2 (UCP2) mRNA, prevented the increase in tumor necrosis factor alpha (TNFα) mRNA, reversed decreases in mitochondrial biogenesis and increased expression of mitochondrial respiratory complexes and manganese superoxide dismutase (MnSOD). The anthocyanins were unique in decreasing ROS without inducing mitochondrial biogenesis or Mn-SOD mRNA expression. In investigations with palmitic acid (Chapter 5), exposure of HepG2 cells to palmitic acid induced endoplasmic reticulum (ER) stress evidenced by upregulated mRNA for the ER chaperones glucose-regulated protein 94 and 78 (GRP94, GRP78) and oxygen-regulated protein 150 (ORP150), cochaperone endoplasmic reticulum-localized DnaJ homologue 4 (ERdj4), and proapoptotic CCAAT-enhancer-binding protein homologous protein (CHOP). A few of the polyphenols (quercetin, catechin, cyanidin) protected against these changes. In a comparison of flavonoids with their phenolic breakdown/digestion products (Chapter 6), the polyphenols 2,4,6-trihydroxybenzaldehyde, protocatechuic acid, and caffeic acid protected similarly to quercetin and cyanidin against oleic and palmitic acid-induced steatosis and ROS generation. Moreover, in a short-term 1 h exposure (to limit spontaneous degradation in the medium), only breakdown/digestion products prevented an oleic acid-induced decrease of mitochondrial biogenesis. In conclusion, different classes of dietary polyphenols were all able to protect against steatosis and ROS generation in this in vitro model of NAFLD. Part of the mechanism for some polyphenols was through effects on mitochondrial biogenesis and function, bioenergetics, and ER stress. Phenolic breakdown/digestion products of flavonoids were shown to contribute to the protective effects of parent polyphenols. Advisors/Committee Members: Bandy, Brian, Arnason, Terra, Paterson, Phyllis, Krol, Edward, Zello, Gordon.

Subjects/Keywords: Non-alcoholic fatty liver disease; Mitochondrial dysfunction; endoplasmic reticulum stress; Steatosis

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APA (6^th Edition):

Rafiei, H. 1. (2017). Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/7946

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Thesis, University of Saskatchewan. Accessed April 21, 2021. http://hdl.handle.net/10388/7946.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Web. 21 Apr 2021.

Vancouver:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Internet] [Thesis]. University of Saskatchewan; 2017. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10388/7946.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Thesis]. University of Saskatchewan; 2017. Available from: http://hdl.handle.net/10388/7946

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

10. Liang, Tian. Molecular Pathogenesis of Dentinogenesis Imperfecta Associated with Dentin Sialophosphoprotein Mutations.

Degree: PhD, Oral Biology, 2018, Texas A&M University

URL: http://hdl.handle.net/1969.1/174013

► Dentin sialophosphoprotein (DSPP) is abundantly expressed by odontoblasts, and transiently expressed by ameloblasts. The mutations in DSPP gene can cause dentinogenesis imperfecta (DGI) type II… (more)

▼ Dentin sialophosphoprotein (DSPP) is abundantly expressed by odontoblasts, and transiently expressed by ameloblasts. The mutations in DSPP gene can cause dentinogenesis imperfecta (DGI) type II (DGI-II) and III (DGI-III), as well as dentin dysplasia (DD) type II (DD-II). To date, 42 DSPP mutations in humans have been identified. However, the molecular pathogenesis has not been determined. We used CRISPR/Cas9 technology to generate a Dspp-KI (knock-in) mouse model, carrying P19L mutation equivalent to the c.50C>T, p.P17L mutation in humans. Compared with wild-type control, the Dsppᴾ¹⁹ᴸ/+ and Dsppᴾ¹⁹ᴸ/ᴾ¹⁹ᴸ (mutant) mice displayed enlarged dental pulp and thinner pulp chamber roof dentin at an early stage, representing DGI-III in humans. With age, the mutant mice showed partial pulp obliteration and thickened pulp chamber floor dentin, resembling DGI-II in humans. The mutant mice also exhibited lower dentin density, defective enamel quality, and compromised dentinoenamel junction. The pathological morphology of odontoblasts and ameloblasts, and the impaired odontoblast processes were observed. Hence, the Dspp-KI mice recapitulated the dentin and enamel phenotypes in human DGI patients. In addition, we discovered reduced DSPP mRNA and accumulated DSPP protein in the odontoblasts and ameloblasts of the mutant mice. The intracellularly accumulated DSPP retained in the endoplasmic reticulum (ER), and activated unfolded protein response (UPR). A UPR branch, inositol-requiring enzyme-1 (IRE1) pathway, was highly activated in the pulp cells of the mutant mice. The activation of IRE1 specifically inhibited the synthesis of DSPP protein during the accumulation of DSPP. Thus, UPR, especially IRE1, may play a major role in DGI associated with DSPP mutations. In summary, we generated a Dspp-KI mouse model recapitulating human DGI, and showed that UPR elicited by the DSPP mutation played a major role in DGI. Further elucidation of the molecular pathogenesis may offer insights for potential treatment plans for DGI. Advisors/Committee Members: Lu, Yongbo (advisor), Qin, Chunlin (committee member), Svoboda, Kathy (committee member), Benson, M. Douglas (committee member), Diekwisch, Thomas (committee member).

Subjects/Keywords: Dentinogenesis Imperfecta; Dentin Sialophosphoprotein; Endoplasmic Reticulum Stress; Unfolded Protein Response

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APA (6^th Edition):

Liang, T. (2018). Molecular Pathogenesis of Dentinogenesis Imperfecta Associated with Dentin Sialophosphoprotein Mutations. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/174013

Chicago Manual of Style (16^th Edition):

Liang, Tian. “Molecular Pathogenesis of Dentinogenesis Imperfecta Associated with Dentin Sialophosphoprotein Mutations.” 2018. Doctoral Dissertation, Texas A&M University. Accessed April 21, 2021. http://hdl.handle.net/1969.1/174013.

MLA Handbook (7^th Edition):

Liang, Tian. “Molecular Pathogenesis of Dentinogenesis Imperfecta Associated with Dentin Sialophosphoprotein Mutations.” 2018. Web. 21 Apr 2021.

Vancouver:

Liang T. Molecular Pathogenesis of Dentinogenesis Imperfecta Associated with Dentin Sialophosphoprotein Mutations. [Internet] [Doctoral dissertation]. Texas A&M University; 2018. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/1969.1/174013.

Council of Science Editors:

Liang T. Molecular Pathogenesis of Dentinogenesis Imperfecta Associated with Dentin Sialophosphoprotein Mutations. [Doctoral Dissertation]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/174013

McMaster University

11. Tat, Victor. THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS.

Degree: MSc, 2017, McMaster University

URL: http://hdl.handle.net/11375/21052

►

Background: Vascular stiffening develops with both hypertension and aging, and is a strong predictor of end-organ damage. Excessive deposition of collagen by vascular smooth muscle… (more)

▼

Background: Vascular stiffening develops with both hypertension and aging, and is a strong predictor of end-organ damage. Excessive deposition of collagen by vascular smooth muscle cells (VSMCs) can lead to decreased compliance of vessels such as the aorta. The IRE1α arm of the unfolded protein response is activated in cells with a secretory phenotype due to its role in augmenting protein folding capacity. We hypothesize that by a similar mechanism, VSMCs transitioning to a collagen-secreting phenotype in response to TGF-β1 require the activation of IRE1. Inhibition of this pathway is hypothesized to reduce collagen secretion and hence prevent the development of fibrosis in the aorta. Methods: Collagen deposition by VSMCs in vitro was measured using immunoblotting and a Picrosirius Red-based colorimetric assay. Western blot and qRT-PCR were used to assess the expression of ER stress markers. Ex vivo culture of aortic rings was also performed to determine the effect of 4µ8c on TGF-β1-induced vascular stiffening. 12-14 week old male spontaneously hypertensive rats were divided into three treatment groups: 1) No treatment, 2) L-NAME (50 mg/L), and 3) L-NAME and the IRE1α inhibitor 4µ8c (2.5 mg/kg/day i.p.). Aortic compliance after 18 days of treatment was measured ex vivo using a wire myograph to construct tension-diameter curves. Results: Inhibition of IRE1α endonuclease activity by 4µ8c reduced collagen production in VSMCs stimulated with TGF-β1 or Ang II. A decrease in the expression of the collagen-associated chaperones PDI, GRP78 and GRP94 was observed. Aortic rings treated with TGF-β1 developed vascular stiffening, which was improved by co-treatment with 4µ8c. SHRs treated with L-NAME for 18 days developed aortic stiffening, which was prevented by daily injections of 4µ8c. Conclusions: Our data suggest that inhibition of the IRE1α pathway can reduce vascular stiffening and fibrosis by disrupting the collagen biosynthesis pathway in VSMCs.

Thesis

Master of Science (MSc)

Advisors/Committee Members: Dickhout, Jeffrey, Medical Sciences (Division of Physiology/Pharmacology).

Subjects/Keywords: Hypertension; Unfolded Protein Response; Endoplasmic Reticulum Stress; Vascular Stiffening; Fibrosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tat, V. (2017). THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/21052

Chicago Manual of Style (16^th Edition):

Tat, Victor. “THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS.” 2017. Masters Thesis, McMaster University. Accessed April 21, 2021. http://hdl.handle.net/11375/21052.

MLA Handbook (7^th Edition):

Tat, Victor. “THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS.” 2017. Web. 21 Apr 2021.

Vancouver:

Tat V. THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS. [Internet] [Masters thesis]. McMaster University; 2017. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/11375/21052.

Council of Science Editors:

Tat V. THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS. [Masters Thesis]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/21052

12. Carlisle, Rachel E. Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis.

Degree: PhD, 2017, McMaster University

URL: http://hdl.handle.net/11375/22040

►

Endoplasmic reticulum (ER) stress, which results from the aggregation of misfolded proteins in the ER, has been implicated in many forms of kidney injury, including… (more)

▼

Endoplasmic reticulum (ER) stress, which results from the aggregation of misfolded proteins in the ER, has been implicated in many forms of kidney injury, including hypertensive nephrosclerosis. ER stress induction increases levels of active TGFβ1, a pro-fibrotic cytokine, which can lead to epithelial-to-mesenchymal transition (EMT) in renal proximal tubular cells. EMT occurs when epithelial cells undergo phenotypic changes, which can be prevented by inhibiting ER stress. Further, the ER stress protein TDAG51 is essential for the development of TGFβ1-mediated fibrosis. The low molecular weight chemical chaperone 4-phenylbutyrate (4-PBA) can protect against ER stress-mediated kidney injury. It acts directly on the kidney, and can prevent ER stress, renal tubular damage, and acute tubular necrosis. In a tunicamycin-mediated model of kidney injury, this damage is prevented primarily through repression of the pro-apoptotic ER stress protein CHOP. Along with providing renoprotective effects, 4-PBA can inhibit endothelial dysfunction and elevated blood pressure in a rat model of essential hypertension. In addition to lowering blood pressure, 4-PBA reduces contractility, augments endothelial-dependent vasodilation, and normalizes media-to-lumen ratio in mesenteric arteries from spontaneously hypertensive rats. Further, ER stress leads to reactive oxygen species generation, which is reduced with 4-PBA. Dahl salt-sensitive rats given 4-PBA are protected from hypertension, proteinuria, albuminuria, and renal pathology. Rats provided with vasodilatory medications demonstrate that lowering blood pressure alone is not renoprotective. In fact, endothelial dysfunction, as demonstrated by an impaired myogenic response, is culpable in the breakdown of the glomerular filtration barrier and subsequent renal damage. As such, alleviating ER stress using 4-PBA serves as a viable therapeutic strategy to preserve renal function and prevent ER stress-mediated endothelial dysfunction, renal fibrosis, glomerular filtration barrier destruction, and progression of hypertensive nephrosclerosis.

Thesis

Doctor of Philosophy (PhD)

Chronic kidney disease is characterized by progressive loss of kidney function, and is a major public health problem. Kidney cells make proteins that help the kidney function properly. However, if the proteins are made improperly, the kidney does not function as well. This can lead to poor filtration and protein in the urine, damage to important kidney structures, and kidney scarring. High blood pressure, a risk factor for kidney disease, is often accused of causing kidney damage. This thesis shows that malfunctioning blood vessels can cause kidney injury, and lowering blood pressure may not prevent this. However, there are pharmacological molecules that can protect the kidney from damage. These molecules help the cells make proteins properly, preventing blood vessel malfunction and kidney damage. Our findings suggest that helping blood vessels and kidney cells create properly functioning proteins is more…

Advisors/Committee Members: Dickhout, Jeffrey G., Medical Sciences (Division of Physiology/Pharmacology).

Subjects/Keywords: endoplasmic reticulum stress; chronic kidney disease; 4-phenylbutyrate; hypertension

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Carlisle, R. E. (2017). Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/22040

Chicago Manual of Style (16^th Edition):

Carlisle, Rachel E. “Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis.” 2017. Doctoral Dissertation, McMaster University. Accessed April 21, 2021. http://hdl.handle.net/11375/22040.

MLA Handbook (7^th Edition):

Carlisle, Rachel E. “Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis.” 2017. Web. 21 Apr 2021.

Vancouver:

Carlisle RE. Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis. [Internet] [Doctoral dissertation]. McMaster University; 2017. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/11375/22040.

Council of Science Editors:

Carlisle RE. Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis. [Doctoral Dissertation]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/22040

NSYSU

13. Tsai, Tsung-Chang. Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells.

Degree: PhD, Institute Of Marine Biotechnology And Resources, 2018, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404

► Cultured soft coral Sinularia sandensis has led to the isolation of elenven natural compounds, including two new cembranoids, 4-carbomethoxyl-10-epigyrosanoldie E (1) and 7-acetylsinumaximol B (2);… (more)

▼ Cultured soft coral Sinularia sandensis has led to the isolation of elenven natural compounds, including two new cembranoids, 4-carbomethoxyl-10-epigyrosanoldie E (1) and 7-acetylsinumaximol B (2); four known cembranoids, sinumaximol B (3), sinulacembranolide A (4), pukalide (5) and 10-epigyrosanolide E (6); two known furanosesquiterpene compounds, methyl (1â²E, 5â²E)-5-(2â²,6â²-dimethylocta-1â²,5â²,7â²-trienyl) furan-3-carboxylate (7) and (1â²E,5â²E)-5-(2â²,6â²-dimethylocta-1â²,5â²,7â²-trienyl)furan-3- carboxylic acid (8); three known steroids, 24-methylenecholestane-3Î²,5Î±,6Î²-triol (9), 11Î±-acetoxy-24-methylenecholesta-3Î²,5Î±,6Î²-triol (10) and 11Î±-acetoxy-24- methylenecholesta-1Î±,3Î²,5Î±,6Î²-tetraol (11). The structures of compounds 1â11 were elucidated by means of IR, MS and NMR techniques, and the absolute configurations of 1 and 5 were further confirmed by single-crystal X-ray diffraction analysis. 7-Acetylsinumaximol B (2) exerted a concentration-dependent anti-proliferative effect on human gastric cancer cells NCI-N87. Activation of mitochondria-related apoptosis was associated with the release of cytochrome c from mitochondria, activation of pro-apoptotic proteins (Bax and Bad) and inhibition of anti-apoptotic proteins (Bcl-2, Bcl-xL, and Mcl-1). Compound 2 triggered endoplasmic reticulum stress, leading to activation of the PERK/elF2Î±/ATF4/CHOP signal pathway. Compound 2 initiated autophagic apoptosis and induced the expression of autophagy-related proteins (Atg3, Atg5, Atg7, Atg12, LC3-I and LC3-II). Our results suggested that compound 2 has the potential to be developed as a useful anti-cancer drug for the treatment of human gastric cancer. Dihydroaustrasulfone alcohol (12) provided a concentration-dependent inhibitory effect on the invasion and migration of human renal cancer cells. The expressions of MMP-2ãMMP-9 and uPA were decreased and TIMP-1 and TIMP-2 were increased. Compound 12 suppressed FAK/PI3K/Akt/mTOR and MAPKs (JNK/p38MAPK/ERK) signal pathway. We concluded that compound 12 has anti-invasion and anti-migration activity of human renal cancer cells 780-O and might be applied to clinical treatment for metastasis of human renal cell carcinoma. Advisors/Committee Members: Jui-Hsin Su (chair), Chih-Chuang Liaw (chair), Ching-Ju Weng (chair), Jyh-Horng Sheu (committee member), Yu-Jen Wu (chair).

Subjects/Keywords: apoptosis; endoplasmic reticulum stress; configuration; autophagy; migration; invasion

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APA (6^th Edition):

Tsai, T. (2018). Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404

Chicago Manual of Style (16^th Edition):

Tsai, Tsung-Chang. “Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells.” 2018. Doctoral Dissertation, NSYSU. Accessed April 21, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404.

MLA Handbook (7^th Edition):

Tsai, Tsung-Chang. “Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells.” 2018. Web. 21 Apr 2021.

Vancouver:

Tsai T. Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells. [Internet] [Doctoral dissertation]. NSYSU; 2018. [cited 2021 Apr 21]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404.

Council of Science Editors:

Tsai T. Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells. [Doctoral Dissertation]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404

University of California – San Francisco

14. Merksamer, Philip Ian. The Development and Application of Fluorescent Protein Reporters to Measure Endoplasmic Reticulum Stress in Single Cells.

Degree: Cell Biology, 2010, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/1dw4d3hd

► In eukaryotic cells, secreted and membrane proteins fold within the endoplasmic reticulum (ER). Various physiological or pathophysiological conditions can disrupt ER protein folding homeostasis and… (more)

Subjects/Keywords: Cellular Biology; endoplasmic reticulum stress; fluorescent protein reporters; unfolded protein response

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APA (6^th Edition):

Merksamer, P. I. (2010). The Development and Application of Fluorescent Protein Reporters to Measure Endoplasmic Reticulum Stress in Single Cells. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/1dw4d3hd

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Merksamer, Philip Ian. “The Development and Application of Fluorescent Protein Reporters to Measure Endoplasmic Reticulum Stress in Single Cells.” 2010. Thesis, University of California – San Francisco. Accessed April 21, 2021. http://www.escholarship.org/uc/item/1dw4d3hd.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Merksamer, Philip Ian. “The Development and Application of Fluorescent Protein Reporters to Measure Endoplasmic Reticulum Stress in Single Cells.” 2010. Web. 21 Apr 2021.

Vancouver:

Merksamer PI. The Development and Application of Fluorescent Protein Reporters to Measure Endoplasmic Reticulum Stress in Single Cells. [Internet] [Thesis]. University of California – San Francisco; 2010. [cited 2021 Apr 21]. Available from: http://www.escholarship.org/uc/item/1dw4d3hd.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Merksamer PI. The Development and Application of Fluorescent Protein Reporters to Measure Endoplasmic Reticulum Stress in Single Cells. [Thesis]. University of California – San Francisco; 2010. Available from: http://www.escholarship.org/uc/item/1dw4d3hd

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – San Francisco

15. Lerner, Alana Gabrielle. Investigation of apoptosis under endoplasmic reticulum stress during diabetes pathogenesis.

Degree: Biomedical Sciences, 2011, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/6b79d4gk

► Diabetes mellitus is a disease caused by a combination of insulin resistance and decline of &beta-cell function. There is a high demand on the pancreatic… (more)

▼ Diabetes mellitus is a disease caused by a combination of insulin resistance and decline of &beta-cell function. There is a high demand on the pancreatic &beta-cell to synthesize and secrete appropriate amounts of insulin in response to glucose levels. When the protein folding demand exceeds the folding capacity of the endoplasmic reticulum (ER), this results in a condition known as ER stress. The cell responds to ER stress by activating an adaptive signaling pathway called the unfolded protein response (UPR). The UPR first tries to restore homeostasis to the cell by reducing the load of proteins to be folded as well as by increasing the folding capacity of the cell. However, if ER stress is chronic, the UPR switches from a homeostatic pathway to an apoptotic pathway. The molecular mechanisms that guide this switch from adaptation to death remain unclear. Elucidating the underlying mechanism of ER stress induced apoptosis would allow better insight for future development of drugs that could prevent cell death and treat diseases such as diabetes. By utilizing mutations in different domains of the ER stress sensor IRE1&alpha, we were able to induce expression of IRE1&alpha mutants in &beta-cells and look at effects on cell fate. By using flow cytometry and microarray analysis we found that chronic IRE1&alpha overexpression resulted in downregulation of hundreds of mRNAs that localize to the ER or secretory pathway, which we hypothesize destabilizes the ER and mediates apoptosis. We also found that IRE1&alpha overexpression alone results in apoptosis, but expression of either kinase dead or RNase dead mutants of IRE1&alpha did not result in downregulation of mRNAs nor apoptosis. These findings uncovered a novel mechanism whereby IRE1&alpha has not only a cytoprotective function, but a proapoptotic arm as well, which requires both its kinase and RNase activity. Continuing this work, we found that TXNIP is a downstream proapoptotic mediator of ER stress apoptosis induced by IRE1&alpha that promotes oxidative stress and cell death. Through these novel findings, we have gained further insight on the mechanism of ER stress mediated apoptosis and also found a convergence of the oxidative stress and ER stress pathways.

Subjects/Keywords: Biology; apoptosis; diabetes; endoplasmic reticulum stress; IRE1; TXNIP

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APA (6^th Edition):

Lerner, A. G. (2011). Investigation of apoptosis under endoplasmic reticulum stress during diabetes pathogenesis. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/6b79d4gk

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lerner, Alana Gabrielle. “Investigation of apoptosis under endoplasmic reticulum stress during diabetes pathogenesis.” 2011. Thesis, University of California – San Francisco. Accessed April 21, 2021. http://www.escholarship.org/uc/item/6b79d4gk.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lerner, Alana Gabrielle. “Investigation of apoptosis under endoplasmic reticulum stress during diabetes pathogenesis.” 2011. Web. 21 Apr 2021.

Vancouver:

Lerner AG. Investigation of apoptosis under endoplasmic reticulum stress during diabetes pathogenesis. [Internet] [Thesis]. University of California – San Francisco; 2011. [cited 2021 Apr 21]. Available from: http://www.escholarship.org/uc/item/6b79d4gk.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lerner AG. Investigation of apoptosis under endoplasmic reticulum stress during diabetes pathogenesis. [Thesis]. University of California – San Francisco; 2011. Available from: http://www.escholarship.org/uc/item/6b79d4gk

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – San Francisco

16. Gardner, Brooke Meghan. Direct Binding to Unfolded Proteins Activates Ire1 and the Unfolded Protein Response.

Degree: Biochemistry and Molecular Biology, 2012, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/5vh5b89b

► Secreted and transmembrane proteins enter the endoplasmic reticulum (ER) as unfolded, nascent polypeptides. Before they continue along the secretory pathway to their final destination, these… (more)

▼ Secreted and transmembrane proteins enter the endoplasmic reticulum (ER) as unfolded, nascent polypeptides. Before they continue along the secretory pathway to their final destination, these proteins must fold into their proper structure. The ER is the primary site of quality control for these proteins; terminally misfolded proteins are degraded, while properly folded proteins are packaged into vesicles. This quality control ensures proper folding, and thus proper function, for all of the proteins that mediate cell-environment interactions. However, the mechanisms required for quality control can also cause an accumulation of unfolded proteins when environmental stresses, developmental programs, or drug treatments disrupt protein folding. Cells facing such ER stress activate a signaling pathway, the Unfolded Protein Response (UPR), designed to restore protein folding homeostasis.In S. cerevisiae, the UPR is activated by the transmembrane protein, Ire1, which initiates a transcriptional program to increase the size and capacity of the ER. Ire1 consists of a stress-sensing lumenal domain that oligomerizes in response to ER stress and cytoplasmic domains that transmit signals to the nucleus and cytoplasm. Ire1 and its activation by oligomerization are conserved throughout the Metazoa. Despite the ubiquity of the UPR pathway and its relevance to human disease, the mechanism of Ire1 stress-sensing and subsequent oligomerization were largely unknown. In Chapter Two, we provide biochemical evidence that unfolded proteins are ligands for Ire1 activation by showing that Ire1 forms a complex in vivo with a model misfolded protein, binds short peptide proxies in vitro, and that peptide binding causes Ire1 oligomerization. Chapter Three extends our findings with Ire1 cLD from S. cerevisiae to the Ire1 lumenal domain from Mus musculus. Although the crystal structure of MmIre1 LD revealed a narrower binding groove, we found that MmIre1 LD can also bind peptides in vitro, but with a different binding preference than ScIre1 cLD. In Chapter Four, we crystallized the lumenal domain of the Ire1 homolog from a thermophilic yeast, Chaetomium thermophilum. This structure reveals several intriguing new interactions within the crystal lattice, which may be important for Ire1 activation.

Subjects/Keywords: Biochemistry; Cellular biology; endoplasmic reticulum; Ire1; stress sensing; Unfolded Protein Response

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APA (6^th Edition):

Gardner, B. M. (2012). Direct Binding to Unfolded Proteins Activates Ire1 and the Unfolded Protein Response. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/5vh5b89b

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gardner, Brooke Meghan. “Direct Binding to Unfolded Proteins Activates Ire1 and the Unfolded Protein Response.” 2012. Thesis, University of California – San Francisco. Accessed April 21, 2021. http://www.escholarship.org/uc/item/5vh5b89b.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gardner, Brooke Meghan. “Direct Binding to Unfolded Proteins Activates Ire1 and the Unfolded Protein Response.” 2012. Web. 21 Apr 2021.

Vancouver:

Gardner BM. Direct Binding to Unfolded Proteins Activates Ire1 and the Unfolded Protein Response. [Internet] [Thesis]. University of California – San Francisco; 2012. [cited 2021 Apr 21]. Available from: http://www.escholarship.org/uc/item/5vh5b89b.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gardner BM. Direct Binding to Unfolded Proteins Activates Ire1 and the Unfolded Protein Response. [Thesis]. University of California – San Francisco; 2012. Available from: http://www.escholarship.org/uc/item/5vh5b89b

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – San Francisco

17. Wang, Eric. The Role of Apoptosis in Differentiation and Disease.

Degree: Biomedical Sciences, 2015, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/3v92x78c

► Apoptosis is a highly conserved form of programmed cell death in multicellular organisms where a cell activates caspase proteases to trigger its own demise. It… (more)

▼ Apoptosis is a highly conserved form of programmed cell death in multicellular organisms where a cell activates caspase proteases to trigger its own demise. It has critical functions under physiological conditions in removing superfluous or damaged cells from a healthy organism. However, dysregulated apoptosis plays an important role in diseases: improper or elevated apoptosis leads to diseases of cell loss, such as diabetes or neurodegeneration, while deficiencies in apoptosis can contribute to tumor cell growth and survival.While the importance of apoptosis during late embryogenesis is well-established, its function during the earliest stages of development, namely the exit of embryonic stem cells (ESC) from the pluripotent state, is unclear. Here, I discovered that apoptosis plays a critical role in removing slow-differentiating murine ESC from the total cell population. This is initiated by p53-dependent upregulation of the Fas death receptor on straggling ESCs, which then triggers apoptosis specifically in these cells. An inability to initiate apoptosis, by transient knockdown or genetic deletion of components of this pathway, causes retention of slow-differentiating ESCs and a global delay in differentiation, both in vitro and in an in vivo teratoma model. Thus, apoptosis is crucial in promoting the efficient differentiation of ESCs.While apoptosis is important for normal development, elevated levels due to cellular stress can cause inappropriate cell loss and degeneration, leading to disease. One such example is retinitis pigmentosa, an inherited disease where rod photoreceptors are progressively lost from the neural retina, eventually leading to blindness. There is increasing evidence that accumulation of unfolded proteins within the endoplasmic reticulum (ER) of rod photoreceptors causes ER stress and subsequent cell death. Here, I utilize a novel small molecule inhibitor to show that inhibition of IRE1α, an ER transmembrane kinase/endoribonuclease that can signal both adaptation and apoptosis in response to ER stress, preserves rod photoreceptor viability and function in two rodent models of ER stress-induced photoreceptor degeneration.These findings reveal new insights into the role of apoptosis under both normal and stressed conditions, and may have implications for human diseases such as cancer and neurodegeneration.

Subjects/Keywords: Biology; Apoptosis; Embryonic Stem Cell; Endoplasmic reticulum stress; IRE1α; Retinitis pigmentosa

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wang, E. (2015). The Role of Apoptosis in Differentiation and Disease. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/3v92x78c

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wang, Eric. “The Role of Apoptosis in Differentiation and Disease.” 2015. Thesis, University of California – San Francisco. Accessed April 21, 2021. http://www.escholarship.org/uc/item/3v92x78c.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wang, Eric. “The Role of Apoptosis in Differentiation and Disease.” 2015. Web. 21 Apr 2021.

Vancouver:

Wang E. The Role of Apoptosis in Differentiation and Disease. [Internet] [Thesis]. University of California – San Francisco; 2015. [cited 2021 Apr 21]. Available from: http://www.escholarship.org/uc/item/3v92x78c.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wang E. The Role of Apoptosis in Differentiation and Disease. [Thesis]. University of California – San Francisco; 2015. Available from: http://www.escholarship.org/uc/item/3v92x78c

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

National University of Ireland – Galway

18. Saveljeva, Svetlana. Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death .

Degree: 2014, National University of Ireland – Galway

URL: http://hdl.handle.net/10379/4786

► This PhD thesis describes cellular responses to the induction of endoplasmic reticulum (ER) stress, focusing on the role of autophagy and cell death. Pro-survival role… (more)

Subjects/Keywords: Endoplasmic reticulum stress; Cell death; Autophagy; Apoptosis; Necroptosis; Biochemistry

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APA (6^th Edition):

Saveljeva, S. (2014). Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/4786

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Saveljeva, Svetlana. “Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death .” 2014. Thesis, National University of Ireland – Galway. Accessed April 21, 2021. http://hdl.handle.net/10379/4786.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Saveljeva, Svetlana. “Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death .” 2014. Web. 21 Apr 2021.

Vancouver:

Saveljeva S. Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death . [Internet] [Thesis]. National University of Ireland – Galway; 2014. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10379/4786.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Saveljeva S. Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death . [Thesis]. National University of Ireland – Galway; 2014. Available from: http://hdl.handle.net/10379/4786

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of the Western Cape

19. Pillay, Leeshan. The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells .

Degree: 2015, University of the Western Cape

URL: http://hdl.handle.net/11394/4459

► Purpose: One of the leading causes of death reported in women worldwide is breast cancer. Manytumours, including breast cancer, associated with poor prognosis, have received… (more)

▼ Purpose: One of the leading causes of death reported in women worldwide is breast cancer. Manytumours, including breast cancer, associated with poor prognosis, have received a renewed focus and increased perspective with regard to drug discovery and innovation towards developing rational combination regimens of first-line anticancer drugs with novel compounds that target diverse hallmarks of the cancer phenotype. Multidrug resistance (MDR), which has been found to significantly decrease the efficacy of anticancer drugs and causes tumor recurrence, has been a major challenge in clinical cancer treatment with chemotherapeutic drugs for decades. Several mechanisms of overcoming drug resistance have been postulated and the well known P-glycoprotein (P-gp) including other drug efflux transporters are considered to be critical in pumping anticancer drugs out of cells which in turn results in unsuccessful chemotherapy treatments. The endoplasmic reticulum (ER) is an interconnecting organelle which synthesizes proteins and its quality control processes ensures the proper protein folding, post-translational modifications and conformation of secretory and trans-membrane proteins. Previous studies demonstrated that geldanamycin (GA), a benzoquinone ansamycin antibiotic, the antibiotic, tunicamycin (TM) and the sesquiterpene lactone, thapsigargin (TG) have been found to cause ER stress and consequently, cellular arrest. GA is known to manifest anti-cancer activity through the inhibition of Hsp90-chaperone, TM interferes with N-glycosylation of newly synthesized proteins triggering the unfolded protein response, while TG inhibits intracellular Ca2+ ATPases resulting in increased cytosolic Ca2+. Cellular stress conditions, lead to accumulation of unfolded or misfolded proteins in the endoplasmic reticulum lumen which results in a unfolded protein response (UPR) to maintain cell survival in cancer cells. ERS has been previously reported to enhance MDR1 transcriptional induction and P-gp transport function in cancer cells, however, prolonged endoplasmic reticulum stress conditions and inadequate unfolded protein response force cells undergo apoptosis. In this study, we examined the effects of GA, TG and TM alone and in combination to determine the cellular response of the MCF-7 breast carcinoma cell line with regard to proliferation and P-gp-mediated drug efflux activity and apoptosis. Methods: Analyses of MCF-7 breast carcinoma cells exposed to Endoplasmic Reticulum Stress (ERS) inducers geldanamycin, thapsigargin and tunicamycin, alone and in combination, included growth curves alone and in the presence of 24 hour IC50 inhibitory concentrations of the 3 ERS inducers alone, dose-response curves (MTT cytotoxicity assays) of the ERS alone and in combination, analysis of P-glycoprotein-mediated efflux pump activity in the presence of the ERS inducers alone and in combination (Calcein-AM efflux assays), analysis of viability, cytotoxicity and early apoptosis via caspase-3/7 expression (Triplex assay) and morphological staining of… Advisors/Committee Members: Hiss, D (advisor).

Subjects/Keywords: Breast cancer; P-Glycoprotein; Apoptosis; Endoplasmic reticulum stress; Multidrug resistance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pillay, L. (2015). The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/4459

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pillay, Leeshan. “The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells .” 2015. Thesis, University of the Western Cape. Accessed April 21, 2021. http://hdl.handle.net/11394/4459.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pillay, Leeshan. “The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells .” 2015. Web. 21 Apr 2021.

Vancouver:

Pillay L. The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells . [Internet] [Thesis]. University of the Western Cape; 2015. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/11394/4459.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pillay L. The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells . [Thesis]. University of the Western Cape; 2015. Available from: http://hdl.handle.net/11394/4459

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

20. Dauer, Patricia. Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer.

Degree: PhD, Pharmacology, 2018, University of Minnesota

URL: http://hdl.handle.net/11299/198397

► Pancreatic ductal adenocarcinoma (PDAC) ranks among the poorest prognoses for cancer patients, with an estimated 5-year survival of just 8%. The stagnant survival rates are… (more)

▼ Pancreatic ductal adenocarcinoma (PDAC) ranks among the poorest prognoses for cancer patients, with an estimated 5-year survival of just 8%. The stagnant survival rates are a result of late detection, chemoresistance, and an aggressive tumor phenotype. Too few patients are eligible for surgery, which results in an urgent need for more effective chemotherapeutic treatment options. One promising pharmacological advancement is currently undergoing a Phase II clinical trial and has been studied by our laboratory. Triptolide is a Chinese herb, which has shown to be very effective in eliminating pancreatic cancer cells in vitro and in vivo. In conjunction with the Medicinal Chemistry Department at the University of Minnesota, a prodrug of triptolide, named Minnelide™, has been synthesized. Our laboratory has since studied triptolide and Minnelide™ extensively, in order to determine the mechanisms of action. The initial study in this dissertation precipitated based on an earlier finding in the Saluja laboratory that triptolide not only downregulates heat shock protein 70 (HSP70) and specificity protein 1 (SP1), but also causes chronic endoplasmic reticulum (ER) stress and cell death. Our study shows that downregulating SP1, a transcription factor that is overexpressed in pancreatic cancer, activates the unfolded protein response (UPR) and results in chronic ER stress. We further show that inhibition of SP1, as well as inducing ER stress, leads to lysosomal membrane permeabilization (LMP), a sustained accumulation of cytosolic calcium, and eventually cell death in pancreatic cancer. Even though ER stress can result in cell death, it is initially a homeostatic mechanism, which aims to protect cells. This led us to ask what role acute ER stress and UPR plays in pancreatic cancer. We show that modulating glucose regulatory protein 78 (GRP78), the master regulator of the UPR, can have a profound effect on multiple pathways that mediate chemoresistance. Our study showed for the first time that knockdown of GRP78 can diminish efflux activity of ATP-binding cassette (ABC) transporters, and it can decrease the antioxidant response resulting in an accumulation of reactive oxygen species (ROS). We also show that these effects can be mediated by the activity of SP1. Our investigation into acute ER stress led to further studies to characterize the UPR signaling in pancreatic cancer. We show that shGRP78 dysregulates multiple transcriptomic and proteomic pathways important in cancer (proliferation, survival, fatty acid metabolism). GRP78 downregulation decreases stemness and self-renewal properties in vitro. In vivo studies demonstrate that GRP78 knockdown results in delayed tumor initiation, and decreased tumor growth. Further, downregulation of GRP78 results in fatty acid metabolism dysregulation. The last study in this dissertation focuses on the tumor microenvironment and SP1 oncogenic signaling. We evaluated the transcriptomic profiling conducted after treatment with triptolide revealed deregulation of the transforming growth…

Subjects/Keywords: Chemoresistance; Endoplasmic Reticulum Stress; GRP78; Pancreatic Cancer; SP1; Tumor microenvironment

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dauer, P. (2018). Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/198397

Chicago Manual of Style (16^th Edition):

Dauer, Patricia. “Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer.” 2018. Doctoral Dissertation, University of Minnesota. Accessed April 21, 2021. http://hdl.handle.net/11299/198397.

MLA Handbook (7^th Edition):

Dauer, Patricia. “Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer.” 2018. Web. 21 Apr 2021.

Vancouver:

Dauer P. Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer. [Internet] [Doctoral dissertation]. University of Minnesota; 2018. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/11299/198397.

Council of Science Editors:

Dauer P. Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer. [Doctoral Dissertation]. University of Minnesota; 2018. Available from: http://hdl.handle.net/11299/198397

University of Southern California

21. Ashish Anshu, Fnu. Anti-cancer effects of novel glidobactin type proteasome inhibitors.

Degree: MS, Molecular Microbiology & Immunology, 2011, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839

► Proteasome inhibitors are widely used today as an important tool for anti-cancer treatment, which has led to a wide search of novel proteasome inhibitors. Proteasome… (more)

Subjects/Keywords: apoptosis; autophagy; endoplasmic reticulum stress; glidobactin A; hematological malignancy; proteasome

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APA (6^th Edition):

Ashish Anshu, F. (2011). Anti-cancer effects of novel glidobactin type proteasome inhibitors. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839

Chicago Manual of Style (16^th Edition):

Ashish Anshu, Fnu. “Anti-cancer effects of novel glidobactin type proteasome inhibitors.” 2011. Masters Thesis, University of Southern California. Accessed April 21, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839.

MLA Handbook (7^th Edition):

Ashish Anshu, Fnu. “Anti-cancer effects of novel glidobactin type proteasome inhibitors.” 2011. Web. 21 Apr 2021.

Vancouver:

Ashish Anshu F. Anti-cancer effects of novel glidobactin type proteasome inhibitors. [Internet] [Masters thesis]. University of Southern California; 2011. [cited 2021 Apr 21]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839.

Council of Science Editors:

Ashish Anshu F. Anti-cancer effects of novel glidobactin type proteasome inhibitors. [Masters Thesis]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839

22. Lhomond, Stephanie. Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas.

Degree: Docteur es, Biologie Cellulaire et Physiopathologie, 2014, Bordeaux

URL: http://www.theses.fr/2014BORD0038

►

Dans les cellules eucaryotes, des altérations du microenvironnement cellulaire ou desmutations des protéines de la voie de sécrétion induisent un stress du RE et activent… (more)

▼

Dans les cellules eucaryotes, des altérations du microenvironnement cellulaire ou desmutations des protéines de la voie de sécrétion induisent un stress du RE et activent uneréponse adaptative nommée UPR. Les signaux intracellulaires associés à l’UPR sont transmisde la lumière du RE vers le noyau par trois protéines transmembranaires dont IRE1α aussiappelée ERN1. Lors d'un stress du RE, IRE1α s'oligomérise, activant ses domaines kinase etendoribonucléase desquelles découle une signalisation intracellulaire complexe. Denombreuses études reliant l'UPR au cancer désignent IRE1α comme un acteur majeur de latumorigenèse, en particulier dans la croissance et la vascularisation des glioblastomes (GBM),bien que les mécanismes précis mis en jeu restent à déterminer. Des études menées dans notrelaboratoire ont identifié deux cibles de l'activité endoribonucléase d'IRE1α (RIDD) : SPARCet PER1, comme effecteurs respectifs des effets pro-migratoire, pro-angiogénique et proprolifératifd'IRE1α dans les GBM. De plus, ces dernières années, le séquençage d'IRE1α apermis d'identifier environ cinquante mutations, dont quatre non silencieuses ont étéidentifiées dans des biopsies de GBM. L'expression de ces quatre mutations, dont A414Tidentifiée dans le laboratoire, dans les cellules U-87 MG, et l'implantation de ces cellules dansle cerveau de souris a permis de mettre en évidence le rôle pro tumoral de la mutation A414Tet le rôle anti-tumoral de la mutation P336L. A414T stabilise les oligomères d'IRE1α, suractivantles voies de signalisation en aval et conduisant à une croissance plus rapide et unevascularisation plus importante des tumeurs. Ainsi, nos travaux confirment qu'IRE1α est unrégulateur central du développement des GBM et pourrait constituer un marqueur pronostic etune cible thérapeutique des GBM.

In eukaryotic cells, alterations in the cellular microenvironment or mutations in the protein secretory pathway induce ER stress and activate an adaptive response termed UPR. The intracellular signals associated with UPR are transmitted from the ER lumen to the nucleus by three transmembrane proteins among which IRE1α also called ERN1. During ER stress, IRE1α oligomerizes, activating its kinase and endoribonuclease domains and a downstream complex intracellular signaling. Many studies linking the UPR to cancer point to IRE1α as a major player in tumorigenesis, particularly in the growth and vascularization of glioblastomas (GBM), although the precise mechanisms involved remain to be determined. Studies led in our laboratory have identified two targets of IRE1α endoribonuclease activity (RIDD): SPARC and PER1 as respective effectors of pro–angiogenic, pro-migratory and proproliferative effects of IRE1α in GBM. In addition, in recent years, IRE1α sequencing identified around fifty mutations, four of which have been identified in GBM biopsies. The expression of these four mutations, including A414T identified in the laboratory, in the U-87 MG cells, and implantation of these cells into mouse brain has highlighted the pro-tumoral role…

Advisors/Committee Members: Chevet, Eric (thesis director).

Subjects/Keywords: Réticulum endoplasmique; Stress; IRE1α; ERN1; Cancer; Glioblastome; Endoplasmic reticulum; Stress; IRE1α; ERN1; Cancer; Glioblastoma

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lhomond, S. (2014). Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas. (Doctoral Dissertation). Bordeaux. Retrieved from http://www.theses.fr/2014BORD0038

Chicago Manual of Style (16^th Edition):

Lhomond, Stephanie. “Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas.” 2014. Doctoral Dissertation, Bordeaux. Accessed April 21, 2021. http://www.theses.fr/2014BORD0038.

MLA Handbook (7^th Edition):

Lhomond, Stephanie. “Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas.” 2014. Web. 21 Apr 2021.

Vancouver:

Lhomond S. Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas. [Internet] [Doctoral dissertation]. Bordeaux; 2014. [cited 2021 Apr 21]. Available from: http://www.theses.fr/2014BORD0038.

Council of Science Editors:

Lhomond S. Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas. [Doctoral Dissertation]. Bordeaux; 2014. Available from: http://www.theses.fr/2014BORD0038

RMIT University

23. Sun, R. The role of ER stress in lipogenesis and insulin resistance in response to over nutrition.

Degree: 2014, RMIT University

URL: http://researchbank.rmit.edu.au/view/rmit:161524

► Insulin resistance is one of the major defect of type 2 diabetes. Excess lipid and endoplasmic reticulum (ER) stress have been suggested to induce hepatic… (more)

▼ Insulin resistance is one of the major defect of type 2 diabetes. Excess lipid and endoplasmic reticulum (ER) stress have been suggested to induce hepatic insulin resistance. However, the mechanisms of the development of insulin resistance relating to excess lipid or ER stress remain unclear. The aims of the thesis were to investigate: 1) the role of ER stress in lipogensis and development of hepatic insulin resistance and, 2) the relationship between ER stress and lipogenesis. The first study was to determine the contribution of ER stress and excess lipid on the onset of hepatic insulin resistance in high fructose (HFru)-fed mice. After feeding with HFru for one day, IRE1/XBP1 branch of the ER stress was activated. Simultaneously, lipogenic enzymes, transcription factor and triglyceride content in the liver increased. Insulin-stimulated phosphorylated Akt was suppressed. Blocking IRE1 activity by TUDCA abolished fructose-dependent increases in JNK activity and IRS serine phosphorylation, and improved Akt phosphorylation without altering hepatic steatosis or PKCϵ. The second study was to interrogate the role of excess lipid or JNK in hepatic insulin resistance in HFru-fed mice. Mice were fed with HFru for 2 weeks. Fenofibrate (FB), a PPARα agonist, was administrated to reduce lipid accumulation. FB treatment eliminated glucose intolerance, hepatic steatosis and insulin signaling transduction. Both IRE1/XBP1 and PEKR/eIF2α branches of ER stress were activated. FB administration increased fatty acid oxidation and reduced diacyglycerols levels. The results from these HFru studies suggested that: 1) ER stress and lipogenesis both contribute to HFru-induced hepatic insulin resistance; 2) activation of JNK rather than lipid accumulation is a key early trigger of ER stress related hepatic insulin resistance induced by HFru feeding and; 3) lipid accumulation, rather than JNK or IKK activation, is pivotal for ER stress to cause hepatic insulin resistance when the mice were challenged with HFru diet for a long time. To further explore the interaction between ER stress and lipogenesis, fructose was used to induce ER stress in cultured cells. Betulin was applied to cells treated with fructose. Lipogenic enzymes were significantly diminished by betulin. The magnified fructose-induced phosphorylation of IRE1 and eIF2α was not altered, suggesting that increasing lipogenesis does not contribute to the activation of IRE1 and PERK branches in context of fructose. In another study, mice were fed with a high fat (HFat) diet for one day or 2 weeks. Hepatic diacyglycerols were increased in HFat-fed mice. Interestingly, HFat-fed mice did not show activated ER stress. These results indicated that hepatic insulin resistance was induced via different mechanisms in the face of fatty acid influx. These observations also suggested that ER stress is unlikely to result from excess lipid. In summary, ER stress might be more critical at early stage of insulin resistance in the context of HFru feeding and this…

Subjects/Keywords: Fields of Research; Hepatic insulin resistance; Endoplasmic reticulum stress; lipid metabolism; Fructose; Liver

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sun, R. (2014). The role of ER stress in lipogenesis and insulin resistance in response to over nutrition. (Thesis). RMIT University. Retrieved from http://researchbank.rmit.edu.au/view/rmit:161524

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sun, R. “The role of ER stress in lipogenesis and insulin resistance in response to over nutrition.” 2014. Thesis, RMIT University. Accessed April 21, 2021. http://researchbank.rmit.edu.au/view/rmit:161524.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sun, R. “The role of ER stress in lipogenesis and insulin resistance in response to over nutrition.” 2014. Web. 21 Apr 2021.

Vancouver:

Sun R. The role of ER stress in lipogenesis and insulin resistance in response to over nutrition. [Internet] [Thesis]. RMIT University; 2014. [cited 2021 Apr 21]. Available from: http://researchbank.rmit.edu.au/view/rmit:161524.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sun R. The role of ER stress in lipogenesis and insulin resistance in response to over nutrition. [Thesis]. RMIT University; 2014. Available from: http://researchbank.rmit.edu.au/view/rmit:161524

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Utah

24. Moore, Kristin A. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.

Degree: PhD, Biology, 2016, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602

► The endoplasmic reticulum (ER) is a dynamic organelle that is responsible for the folding and quality control of proteins within the endomembrane system. Both physiological… (more)

▼ The endoplasmic reticulum (ER) is a dynamic organelle that is responsible for the folding and quality control of proteins within the endomembrane system. Both physiological and pathological conditions can result in accumulation of misfolded proteins within the ER, a situation termed ER stress, which results in cell death if not alleviated. Perturbations in ER function result in activation of three ER transmembrane proteins (Ire1, Perk, and Atf6) that are primarily responsible for facilitating the unfolded protein response (UPR). Activation of the UPR initially increases ER capacity to offset the surge in misfolded protein; however, during irremediable stress, the UPR activates pro-apoptotic pathways presumably to prevent the cytotoxic consequences of secreting misfolded proteins. Ire1 is an endoribonuclease that is responsible for the unconventional splicing of an intron from the transcription factor, Xbp1. However, Ire1 is also responsible for the direct degradation of a number of mRNAs, a process termed regulated Ire1-dependent decay (RIDD). In mammals, long-term activation of Ire1 results in nonspecific cleavage of ER-localized mRNAs and subsequent cell death. However, at early time points a limited number of mRNAs are prioritized to the RIDD pathway and are degraded relatively rapidly. In the work presented here, I address the questions of (1) how specific mRNAs are prioritized for degradation? And (2) what is the function mRNA degradation during acute of ER stress? I have found that specific nucleotide sequence and structural motifs are used to target mRNAs to the RIDD pathway in both fly and mammalian cells. Furthermore, I show that inhibiting translation of these motifs is also essential for RIDD targeting. Lastly, I show Ire1-dependent effects on lysosome accumulation during ER stress; this may enhance prosurvival signaling of the UPR. These data provide insight into the mechanisms of Ire1 function as well as a model for how the RIDD pathway may function in both the prosurvival and pro-apoptotic pathways of the UPR.

Subjects/Keywords: Blos1; Endoplasmic reticulum (ER); ER stress; mRNA degradation; Regulated-Ire1 Dependent Decay; Unfolded Protein Response

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APA (6^th Edition):

Moore, K. A. (2016). The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602

Chicago Manual of Style (16^th Edition):

Moore, Kristin A. “The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.” 2016. Doctoral Dissertation, University of Utah. Accessed April 21, 2021. http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602.

MLA Handbook (7^th Edition):

Moore, Kristin A. “The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.” 2016. Web. 21 Apr 2021.

Vancouver:

Moore KA. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. [Internet] [Doctoral dissertation]. University of Utah; 2016. [cited 2021 Apr 21]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602.

Council of Science Editors:

Moore KA. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. [Doctoral Dissertation]. University of Utah; 2016. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602

Cornell University

25. Krumm, Christopher Steven. Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse.

Degree: PhD, Animal Science, 2017, Cornell University

URL: http://hdl.handle.net/1813/47862

► The first part of this dissertation assessed factors regulating the insulin sensitizing hormone adiponectin in dairy cows. Plasma adiponectin is reduced during the transition from… (more)

▼ The first part of this dissertation assessed factors regulating the insulin sensitizing hormone adiponectin in dairy cows. Plasma adiponectin is reduced during the transition from late pregnancy (LP) to early lactation (EL) in parallel with rapid changes in the plasma concentration of metabolic hormones [i.e. insulin, leptin, and growth hormone (GH)] and non-esterified fatty acids (NEFA). The first study of this dissertation showed that none of these factors contribute to the regulation of plasma adiponectin. The second study tested the possibility that altered endoplasmic reticulum (ER) chaperone expression is involved. This was motivated by the following observations: 1) Plasma adiponectin variation in transition dairy cows occurs in absence of changes in adiponectin mRNA. 2) In rodents, the master regulator of ER homeostasis x-box binding protein 1 (Xbp1) regulates adiponectin production by increasing ER chaperone expression. We showed that Xbp1 expression decreased from LP to EL in the dairy cow. Using a primary bovine adipocyte system, overexpression of Xbp1 had no effect on adiponectin, despite increasing expression of several ER chaperone proteins. The factors regulating plasma adiponectin in the transition dairy cow remain unknown. The second part of this dissertation addressed the role of sel-1 suppressor of lin-12-like protein (Sel1l) in lipid metabolism. Sel1l is a critical component of the endoplasmic reticulum associated degradation (ERAD) system required for translocation and degradation of misfolded or aggregated proteins. Adipose-specific deletion of Sel1l in mice has implicated an ERAD-independent role for Sel1l in lipid metabolism. To this end, we generated liver-specific Sel1l knockout mice (ΔSel1lLiver) to assess whether Sel1l plays a similar role in lipid homeostasis in liver. Lipid metabolism was nearly normal in ΔSel1lLiver mice fed chow or high fat diet. ΔSel1lLiver mice on an atherogenic diet (AD) showed increased hyperlipidemia, hypercholesterolemia, liver damage, and occasional death compared to wildtype (WT) mice. This phenotype was associated with increased 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr) and decreased low-density lipoprotein receptor (Ldlr) in liver of ΔSel1lLiver mice. Together, our results reveal a previously unknown role for Sel1l in lipid homeostasis in liver, but further studies are needed to elucidate the mechanism. Advisors/Committee Members: Boisclair, Yves R (chair), Lujan, Marla E. (committee member), Van Amburgh, Michael E (committee member), Weiss, Robert S. (committee member).

Subjects/Keywords: Endocrinology; Biology; Adiponectin; endoplasmic reticulum stress; Metabolism; Sel1L; Transition Dairy Cow; Animal sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Krumm, C. S. (2017). Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/47862

Chicago Manual of Style (16^th Edition):

Krumm, Christopher Steven. “Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse.” 2017. Doctoral Dissertation, Cornell University. Accessed April 21, 2021. http://hdl.handle.net/1813/47862.

MLA Handbook (7^th Edition):

Krumm, Christopher Steven. “Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse.” 2017. Web. 21 Apr 2021.

Vancouver:

Krumm CS. Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse. [Internet] [Doctoral dissertation]. Cornell University; 2017. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/1813/47862.

Council of Science Editors:

Krumm CS. Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse. [Doctoral Dissertation]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/47862

Vanderbilt University

26. Leamy, Alexandra Kathlene. Role of lipid metabolic pathways in the progression of hepatic lipotoxicity.

Degree: PhD, Chemical Engineering, 2015, Vanderbilt University

URL: http://hdl.handle.net/1803/11066

► The steady rise in Western obesity rates has been closely linked to significant increases in a multitude of accompanying health problems including obesity, type II… (more)

▼ The steady rise in Western obesity rates has been closely linked to significant increases in a multitude of accompanying health problems including obesity, type II diabetes and non-alcoholic fatty liver disease (NAFLD). NAFLD severity ranges from simple steatosis to acute steatohepatitis, but the molecular mechanisms controlling progression of this disease are poorly understood. The liver plays a central role in whole body homeostasis and, therefore, impairments in hepatic function are detrimental to a variety of biological processes. These hepatic dysfunctions are thought to be triggered by elevated free fatty acid flux from either dietary intake or adipose tissue efflux that results in etopic deposition of fat in the liver. It is known to be accompanied by increased signaling thorough cellular stress pathways, oxidant stress and eventual apoptosis. This phenotype is collectively termed hepatic lipotoxicity. Recent literature suggests that elevated free fatty acids (FFAs), especially saturated fatty acids (SFAs), play a central role in lipotoxic mechanisms, both in experimental models and in NAFLD patients. Relevant cellular processes that have been causally linked to lipotoxicity include endoplasmic reticulum (ER) stress, oxidative stress, mitochondrial dysfunction, and apoptosis. In contrast, increased triglyceride synthesis has been shown to have a protective effect against lipotoxicity, despite being one of the hallmark traits of NAFLD. The overarching theme of this dissertation is designing studies to better understand how the degree of intrahepatic lipid saturation controls cell fate in response to an elevated FFA load and the mechanisms through which these fatty acids act. Our results indicate that disordered phospholipid metabolism, specifically over saturation of membrane bilayers initiates a signaling cascade which culminates in cell death. Interventions designed to prevent saturation of the phospholipids improves hepatic cell fate when in environments of saturated fatty acid overload. Developing a more nuanced understanding of the molecular mechanisms underlying NAFLD progression will lead to more targeted and effective therapeutics for this increasingly prevalent disease, which to date has no proven pharmacologic treatment to prevent or reverse its course. Advisors/Committee Members: M. Douglas LeVan (committee member), David Wasserman (committee member), Scott Guelcher (committee member), Jamey Young (Committee Chair).

Subjects/Keywords: phospholipids; triglyceride synthesis; endoplasmic reticulum stress; saturated fatty acids; lipotoxicity; lipid metabolism

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Leamy, A. K. (2015). Role of lipid metabolic pathways in the progression of hepatic lipotoxicity. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11066

Chicago Manual of Style (16^th Edition):

Leamy, Alexandra Kathlene. “Role of lipid metabolic pathways in the progression of hepatic lipotoxicity.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed April 21, 2021. http://hdl.handle.net/1803/11066.

MLA Handbook (7^th Edition):

Leamy, Alexandra Kathlene. “Role of lipid metabolic pathways in the progression of hepatic lipotoxicity.” 2015. Web. 21 Apr 2021.

Vancouver:

Leamy AK. Role of lipid metabolic pathways in the progression of hepatic lipotoxicity. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/1803/11066.

Council of Science Editors:

Leamy AK. Role of lipid metabolic pathways in the progression of hepatic lipotoxicity. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://hdl.handle.net/1803/11066

North Carolina State University

27. Kirst, Mariana E. Identification and characterization of maize Derlins in response to endoplasmic reticulum stress.

Degree: PhD, Botany, 2007, North Carolina State University

URL: http://www.lib.ncsu.edu/resolver/1840.16/4954

Subjects/Keywords: Derlin; ERAD; ER stress; endoplasmic reticulum

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kirst, M. E. (2007). Identification and characterization of maize Derlins in response to endoplasmic reticulum stress. (Doctoral Dissertation). North Carolina State University. Retrieved from http://www.lib.ncsu.edu/resolver/1840.16/4954

Chicago Manual of Style (16^th Edition):

Kirst, Mariana E. “Identification and characterization of maize Derlins in response to endoplasmic reticulum stress.” 2007. Doctoral Dissertation, North Carolina State University. Accessed April 21, 2021. http://www.lib.ncsu.edu/resolver/1840.16/4954.

MLA Handbook (7^th Edition):

Kirst, Mariana E. “Identification and characterization of maize Derlins in response to endoplasmic reticulum stress.” 2007. Web. 21 Apr 2021.

Vancouver:

Kirst ME. Identification and characterization of maize Derlins in response to endoplasmic reticulum stress. [Internet] [Doctoral dissertation]. North Carolina State University; 2007. [cited 2021 Apr 21]. Available from: http://www.lib.ncsu.edu/resolver/1840.16/4954.

Council of Science Editors:

Kirst ME. Identification and characterization of maize Derlins in response to endoplasmic reticulum stress. [Doctoral Dissertation]. North Carolina State University; 2007. Available from: http://www.lib.ncsu.edu/resolver/1840.16/4954

28. Aydoğdu, Gülizar. Glutamin taşınması ve metabolizmasının insülin direnci ve endoplazmik retikulum stresi üzerindeki rolü: The role of glutamine transport and metabolism in the insulin resistance and endoplasmic reticulum stress.

Degree: Fen Fakültesi, 2019, University of Ankara

URL: http://hdl.handle.net/20.500.12575/70224

► Obezite, son zamanlardaki önemli sağlık problemlemlerinden biridir. Obezitenin tip-2 diyabet riskini arttırdığı ve tip-2 diyabetteki insülin direncinin ortaya çıkışında da endoplazmik retikulum (ER) stresinin katkısının… (more)

▼ Obezite, son zamanlardaki önemli sağlık problemlemlerinden biridir. Obezitenin tip-2 diyabet riskini arttırdığı ve tip-2 diyabetteki insülin direncinin ortaya çıkışında da endoplazmik retikulum (ER) stresinin katkısının olduğu bilinmektedir. Obez bireylerde yüksek miktarlarda bulunan glutaminin insülin direncindeki rolü ile ilgili mekanizmalar yeterince anlaşılabilmiş değildir. Tez kapsamında, insülin direnci durumunda hücre içine glikoz alınamamasının getirdiği enerji ve hammadde eksikliğini gidermede glutamin kullanılıyor olabilir mi sorusuna yanıt aranmaktadır. Glutaminin ve glutaminin taşınmasının, insülin direnci ve ER stresi ile ilişkisini belirlemek amacıyla bu yolaklarda yer alan belirteç proteinlerin seviyeleri ve fosforilasyon düzeyleri western blot yöntemi ile incelenmiştir. Farklılaşmış 3T3-L1 adipositleriyle yapılan deneylerde, artan glutamin uygulamasının insülin hassasiyetini arttırdığı ve ER stresi azalttığı gösterilmiştir. Adipositlerde tunikamisin aracılığıyla ER stres ve insülin direnci uyarıldığında glutamin taşıyıcılarının seviyeleri azalırken, palmitat ile uyarılan ER stres ve insülin direnci durumunda ise glutamin taşıyıcılarınının seviyelerinde artış görülmüştür. Glutamin taşıyıcısı ASCT2'nin ifadesinin azaltıldığı 3T3-L1 fibroblastları adipositlere farklılaştırıldığında, hücre içi yağ birikimi ciddi oranda azalırken beraberinde insülin direnci ve ER stres de azalmaktadır. Ayrıca, hücre içi glutamin, malat ve fumarat düzeyleri kolorimetrik olarak ölçüldüğünde, adiposite farklılaşmanın etkisiyle glutamin ve malat miktarı artmaktadır. ASCT2'nin ifadesinin azaldığı adipositlerde ise glutamin düzeyi düşer iken fumarat ve malat düzeyleri değişmemektedir. Sonuç olarak, adipositlerdeki insülin direnci ile hücre için gerekli enerji ve hammaddelerin glikozdan sağlanamaması durumunda mitokondride glutaminin kullanıldığı bulunmuştur. Önemli bir enerji ve karbon kaynağı olan glutamin insülin direncine etkisini ER stres üzerinden gösterdiği ortaya çıkarılmıştır. Glutamin ve ASCT2'nin obezite ve tip 2 diayabet için geliştirilebilecek tedavi yaklaşımlarında önemli hedefler olduğu gösterilmiştir. Advisors/Committee Members: Aras, Sümer (advisor).

Subjects/Keywords: Endoplazmik retikulum stresi; İnsülin direnci; Glutamin; Endoplasmic reticulum stress; İnsulin resistance; Glutamine

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Aydoğdu, G. (2019). Glutamin taşınması ve metabolizmasının insülin direnci ve endoplazmik retikulum stresi üzerindeki rolü: The role of glutamine transport and metabolism in the insulin resistance and endoplasmic reticulum stress. (Doctoral Dissertation). University of Ankara. Retrieved from http://hdl.handle.net/20.500.12575/70224

Chicago Manual of Style (16^th Edition):

Aydoğdu, Gülizar. “Glutamin taşınması ve metabolizmasının insülin direnci ve endoplazmik retikulum stresi üzerindeki rolü: The role of glutamine transport and metabolism in the insulin resistance and endoplasmic reticulum stress.” 2019. Doctoral Dissertation, University of Ankara. Accessed April 21, 2021. http://hdl.handle.net/20.500.12575/70224.

MLA Handbook (7^th Edition):

Aydoğdu, Gülizar. “Glutamin taşınması ve metabolizmasının insülin direnci ve endoplazmik retikulum stresi üzerindeki rolü: The role of glutamine transport and metabolism in the insulin resistance and endoplasmic reticulum stress.” 2019. Web. 21 Apr 2021.

Vancouver:

Aydoğdu G. Glutamin taşınması ve metabolizmasının insülin direnci ve endoplazmik retikulum stresi üzerindeki rolü: The role of glutamine transport and metabolism in the insulin resistance and endoplasmic reticulum stress. [Internet] [Doctoral dissertation]. University of Ankara; 2019. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/20.500.12575/70224.

Council of Science Editors:

Aydoğdu G. Glutamin taşınması ve metabolizmasının insülin direnci ve endoplazmik retikulum stresi üzerindeki rolü: The role of glutamine transport and metabolism in the insulin resistance and endoplasmic reticulum stress. [Doctoral Dissertation]. University of Ankara; 2019. Available from: http://hdl.handle.net/20.500.12575/70224

29. 정, 익락. The effect of iron metabolism on palmitate-induced INS-1 cell death.

Degree: 2015, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143

►

Ⅰ. INTRODUCTION 1 Ⅱ. MATERIALS AND METHODS 24 A. MATERIALS 24 1. Reagents 24 B. METHODS 25 1. Cell Culture 25 2. Preparation of palmitate… (more)

Subjects/Keywords: Apoptosis; Endoplasmic reticulum(ER) stress; Lipotoxicity; Iron; INS-1 Cell; Palmitate; Transferrin receptor; Soduim fluorocitrate

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

정, �. (2015). The effect of iron metabolism on palmitate-induced INS-1 cell death. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

정, 익락. “The effect of iron metabolism on palmitate-induced INS-1 cell death.” 2015. Thesis, Ajou University. Accessed April 21, 2021. http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

정, 익락. “The effect of iron metabolism on palmitate-induced INS-1 cell death.” 2015. Web. 21 Apr 2021.

Vancouver:

정 �. The effect of iron metabolism on palmitate-induced INS-1 cell death. [Internet] [Thesis]. Ajou University; 2015. [cited 2021 Apr 21]. Available from: http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

정 �. The effect of iron metabolism on palmitate-induced INS-1 cell death. [Thesis]. Ajou University; 2015. Available from: http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Boston University

30. Motomochi, Amanda. Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury.

Degree: MS, Medical Sciences, 2014, Boston University

URL: http://hdl.handle.net/2144/14397

► Enterohemorrhagic E. coli (EHEC) infections are a leading cause of foodborne illness in the United States. Shiga-like toxins are produced that can cause hemorrhagic colitis… (more)

Subjects/Keywords: Pathology; Enterohemorrhagic Escherichia coli; Endoplasmic reticulum stress; Hemolytic uremic syndrome; Shiga-like toxins

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Motomochi, A. (2014). Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/14397

Chicago Manual of Style (16^th Edition):

Motomochi, Amanda. “Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury.” 2014. Masters Thesis, Boston University. Accessed April 21, 2021. http://hdl.handle.net/2144/14397.

MLA Handbook (7^th Edition):

Motomochi, Amanda. “Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury.” 2014. Web. 21 Apr 2021.

Vancouver:

Motomochi A. Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury. [Internet] [Masters thesis]. Boston University; 2014. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/2144/14397.

Council of Science Editors:

Motomochi A. Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury. [Masters Thesis]. Boston University; 2014. Available from: http://hdl.handle.net/2144/14397

Open Access Theses and Dissertations