Dissertations / Theses on the topic 'ER stress'
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Chan, Cheuk-wing Wilson, and 陳卓榮. "ER stress in the pathogenesis of osteochondrodysplasia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085192.
Full textChan, Cheuk-wing Wilson. "ER stress in the pathogenesis of osteochondrodysplasia." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085192.
Full textLo, Ling-kit Rebecca. "ER-stress signaling and chondrocyte differentiation in mice." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B3861926X.
Full textLo, Ling-kit Rebecca, and 羅令潔. "ER-stress signaling and chondrocyte differentiation in mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B3861926X.
Full textAdolph, Timon Erik. "ER stress converts autophagy defects into intestinal inflammation." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708683.
Full textAlves, Inês Sofia Moutinho. "Contribution of ER stress to tumor immunosuppressive microenvironment." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/14290.
Full textBreast cancer is the most prevalent cancer among women and also one of the oncologic pathologies that causes more deaths. In the last decades several studies have reported that solid tumors generate an immunosuppressive microenvironment. This microenvironment (acidosis, hypoxia, glucose deprivation and cytokines) is favourable to endoplasmic reticulum (ER) stress induction. ER stress is primarily a response towards the re-establishment of homeostasis; however if not resolved it usually results in cell death by apoptosis. Nevertheless, ER stress and unfolded protein response (UPR) play a paradoxical role in cancer physiopathology: the three branches of UPR, PERK, IRE1 and ATF6 actively contribute to signalling of survival and metastasis mechanisms. Recently it was reported a possible transmission of ER stress from tumor cells to immune cells, modulating the phenotype and function of recipient cells. Thus, the aim of the present work is to assess the ability and the respective mechanisms by which T-47D tumor cells transmit ER stress to THP-1 monocytes, and the consequences of this transmission. ER stress transmission was only observed when pharmacological ER stress inducers were used, such as tunicamycin, contrarily to physiological stimulation, as glucose deprivation. Additionally, it was found that tunicamycin seems to be transported within exosomes which, in turn, directly induces ER stress on monocytes. It was also observed that exosomes derived from glucose deprived T-47D cells do not transmit ER stress; however these exosomes conduct monocytes towards a particular proinflammatory profile, accompanied by the decrease of its maturation status. Overall, our results question the ER stress mechanism originally described, showing that pharmacological ER stress inducers can be transported within exosomes and directly inducing ER stress on recipient cells.
O cancro da mama é o cancro de maior incidência entre as mulheres, sendo também uma das situações oncológicas que mais mortes causa. Na última década inúmeros estudos têm demonstrado que os tumores sólidos geram um microambiente favorável à evasão/subversão do sistema imune. Esse microambiente (acidose, hipoxia, deprivação de glucose, citoquinas) é muita das vezes propicio à indução de stress do reticulo endoplasmático (RE). O stress do RE é primariamente uma resposta no sentido de restabelecer a homeostasia no entanto se não resolvido resulta normalmente na morte celular por apoptose. O stress do RE e a respetiva resposta às proteínas mal conformadas (UPR), desempenham um papel paradoxal na fisiopatologia do cancro: os três ramos da UPR, PERK, IRE1 e ATF6, contribuem ativamente para a sinalização de alguns mecanismos de sobrevivência e metastização. Recentemente, foi descrita uma possível transmissão do stress do RE das células tumorais para as células do sistema imunitário, modulando a ação destas. Desta forma, pretendeu avaliar-se com o presente trabalho a capacidade e os mecanismos pelos quais células tumorais T-47D transmitem o stress do RE para células monocíticas THP-1, e quais as consequências desta transmissão. A transmissão foi apenas observada aquando da utilização de indutores farmacológicos como a tunicamicina, não se registando para estímulos fisiológicos como a deprivação de glucose. Por outro lado, verificou-se que a tunicamicina parece ser transportada via exossomas e desta forma induzir diretamente stress do RE nos monócitos. Observou-se ainda que os exossomas provenientes das células T-47D em stress do RE por deprivação de glucose apesar de não transmitirem o referido stress conduzem os monócitos para um perfil pró-inflamatório específico diminuindo ainda a sua capacidade de maturação. Em geral, os nossos resultados questionam seriamente o mecanismo de transmissão de stress ER tal como originalmente descrito, mostrando que no uso de indutores farmacológicos o que parece ocorrer é o transporte do fármaco em vesículas e a indução direta nas células recetoras.
Narayanan, Siddharth. "Crosstalk between the ER stress pathway and osmotic stress in S. cerevisiae." Thesis, Durham University, 2011. http://etheses.dur.ac.uk/3435/.
Full textQaisiya, Mohammed Ali Hassan. "UNCONJUGATED BILIRUBIN MEDIATED OXIDATIVE STRESS, ER STRESS, AND ACTIVATION OF NRF2 PATHWAY." Doctoral thesis, Università degli studi di Trieste, 2014. http://hdl.handle.net/10077/10137.
Full textElevati livelli plasmatici di bilirubina non coniugata (UCB) sono responsabili dell’ittero neontale che è fisiologico nella maggior parte dei casi. L’iperbilirubinemia severa e prolungata nel tempo può causare encefalopatia da bilirubina e Kernicterus che, se non trattati, possono lasciare pesanti sequele neurologiche e nei casi più gravi condurre a morte. La neurotossicità da bilirubina è ancora una delle principali cause di malattie neurologiche nei paesi via di sviluppo ed è un problema riemergente nei paesi sviluppati a causa delle anticipate dimissioni dall’ospedale dei neonati. I meccanismi molecolari responsabili della neurotossicità da bilirubina non sono ancora completamente chiariti. Questo lavoro riporta i risultati ottenuti durante il mio progetto di dottorato volto a studiare il “molecular signalling” coinvolto nella neurotossicità da bilirubina. L’obiettivo principale è stato valutare gli effetti di concentrazioni pro-ossidanti di bilirubina sullo stato redox cellulare e sullo stress del reticolo endoplasmico (ER stress). Ci siamo focalizzati sulla pathway che coinvolge Nrf2, analizzando i geni indotti dalla bilirubina per effetto di Nrf2 e studiando il signalling a monte coinvolto nella sua attivazione. Parallelamente abbiamo anche studiato la cascata di segnali coinvolti nell’ER stress. Tutti gli esperimenti sono stati condotti nella linea cellulare di neuroblastoma umano SH-SY5Y, alcuni ripetuti anche nella linea di epatocarcinoma HepG2 e in colture primarie di astrociti dalla corteccia cerebrale di ratto. I nostri risultati mostrano che concentrazioni tossiche di bilirubina inducono un 40% di mortalità cellulare tra 1 e 4 ore di trattamento che si mantiene stabile fino alle 24 ore di trattamento. Le cellule trattate con UCB mostrano un incremento del livello dei ROS intracellulare dopo 1 ora seguito dall’accumulo nucleare dell’Nrf2 endogeno dopo 3 ore. La bilirubina aumenta l’induzione della trascrizione dell’ARE-GFP reporter gene associata ad una up-regolazione di diversi geni target di Nrf2. L’induzione dell’espressione genica può essere suddivisa in due categorie principali:la risposta precoce (4h-8h) e la risposta tardiva (16h-24h).La risposta precoce inizia con l’induzione dell’espressione di ATF3 dopo 4 ore di trattamento ed è seguita da i trasportatori di amminoacidi (xCT and Gly1) dopo 8h. Per la risposta tardiva abbiamo visto l’induzione dell’espressione genica degli enzimi coinvolti nella sintesi del glutatione. (γGCL and TNX1),nella risposta antiossidante e di detossificazione (HO-1, NQO1, FTH)e nell’omeostasi del NADPH (ME1, and G6PD). In seguito al silenziamento specifico di Nrf2, il trattamento con bilirubina diminuisce l’induzione dell’mRNA solo dell’HO-1 (75%), del NQO1 (56%) e della FTH (40%) Inoltre l’induzione dell’HO-1 è ridotta se le cellule vengono pretrattate con l’antiossidante NAC (65%) e con specifici inibitori per PKC (80%), P38α (40%) and MEK1/2 (25%). Risulta evidente che l’induzione di ATF3 è la prima risposta generata dal trattamento con UCB. Di seguito abbiamo osservato un’induzione sequenziale dei marker dell’ER stress: da quelli coinvolti nel signaling di PERK a 4h (PERK, ATF3, ATF4, CHOP), dalla diminuzione della proteina della ciclina D1 dopo 1 h e dall’induzione di IRE1 (XBP1), ATF6, e BiP dopo 8h di trattamento. Da notare però che il silenzia mento di PERK non riduce l’induzione dell’espressione dell’mRNA di ATFs/CHOP, ma induce l’espressione dell’mRNA di GCN2. Riassumendo noi abbiamo dimostrato che la bilirubina causa mortalità cellulare, produce la formazione di ROS, provoca l’accumulo di Nrf2 nel nucleo e induce la risposta antiossidante mediata dalle sequenze ARE. La bilirubina induce l’espressione di diversi geni coinvolti nella risposta antiossidante, tra tutti l’HO-1 e il NQO1 sono indotti dalla bilirubina in maniera dipendente da Nrf2. Abbiamo anche dimostrato che lo stress ossidativo (OS) e la PKC sono i principali fattori coinvolti nell’attivazione di Nrf2/HO-1. I risultati ottenuti dimostrano che l’induzione di ATFs/CHOP e di PERK sono uno dei primi eventi associati alla tossicità da bilirubina. Allo stesso tempo il silenziamento di PERK non influisce sull’induzione di ATFs/CHOP mentre induce GCN2, suggerendo un meccanismo di compensazione tra il signalling di PERK e GCN2. Concludendo i nostri dati dimostrano che lo stress ossidativo e lo stress del reticolo endoplasmico sono coinvolti nella neurotossicità indotta da UCB nella linea di neuroblastoma umano SH-SY5Y. Le cellule sviluppano una risposta adattativa alla bilirubina inducendo OS and ER stress e aumentando l’espressione dei geni coinvolti nella risposta antiossidante (in parte via Nrf2 pathway) e nello stress del reticolo endoplasmico (UPR).
Elevated levels of unconjugated bilirubin (UCB) are responsible for neonatal jaundice, and in some case, severe hyperbilirubinemia exposes babies to bilirubin encephalopathy and kernicterus with the risk of neurological sequela and death. Bilirubin neurotoxicity is still a major cause of neurological injury in the developing countries and is a re-emerged problem in the developed countries, due to the early hospital discharge of newborns after birth. The molecular mechanisms of UCB induced neurotoxicty are incompletely elucidated. Present thesis are reported the results obtained during my PhD course aimed to investigate the molecular signaling involved in UCB induced neurotoxicity .The main goal of this work was to evaluate the effects of the pro-oxidant concentration of UCB on cellular redox state and ER stress. We focused on Nrf2 pathway, analyzing the genes induced by UCB at Nrf2-dependent manner and the up-stream signaling involved in Nrf2 pathway activation. In parallel, we also studied the ER stress cascade signaling. All experiments were conducted in SH-SY5Y neuroblastoma cell line, with some performed in HepG2 cells and primary culture of cortical astrocytes. Our results showed that SH-SY5Y neuroblastoma cells incubated with toxic concentration of UCB suffer a 40% loss of cell viability between 1h to 4h, reaching a plateau until 24h after UCB treatment. Treated cells showed an increased level of intracellular ROS after 1h followed by the nuclear accumulation of endogenous Nrf2 after 3h. UCB enhanced the transcriptional activation of ARE-GFP reporter gene associated with an up-regulation of several Nrf2 target genes. Expression response could be divided into two main categories: early (4h-8h) and late response (16h-24h). As far as early genes, UCB mediates a sequential transcription starting with the ATF3 up-regulation at 4h and followed by the induction of amino acid transporters at 8h (xCT and Gly1). On the contrary, for late genes, we observed an up-regulation of the enzymes involved in GSH synthesis (γGCL and TNX1), antioxidant/detoxification (HO-1, NQO1, FTH), and NADPH homeostasis (ME1, and G6PD). Specific Nrf2 siRNA against Nrf2 decreased the induction only of HO-1 (75%), NQO1 (56%), and FTH (40%) upon UCB exposure. HO-1 induction was reduced in cells pre-treated with antioxidant NAC (65%) and with specific signaling inhibitors for PKC (80%), P38α (40%) and MEK1/2 (25%). It was evident that ATF3 up-regulation at 4h represents the earliest response to UCB exposure. We observed a sequential activation of UPR sensors starting with PERK signaling at 4h (up-regulation of PERK, ATF3, ATF4, CHOP at 4h, and loss of cyclin D1 protein at 1h), followed by IRE1 (XBP1), ATF6, and BiP at 8h after UCB treatment. Interestingly, PERK siRNA does not changed the induction of ATFs/CHOP while induced GCN2 mRNA upon UCB exposure. In summary, we demonstrated that UCB mediates loss of cell viability, ROS generation, Nrf2 nuclear accumulation and induction of ARE. Nrf2 pathway activation was associated with the induction of multiple antioxidant genes, among all, HO-1 and NQO1 are induced by UCB at Nrf2-dependent manner. We observed that OS and PKC are the major up-stream signaling involved in Nrf2/HO-1 activation. Results demonstrated ATFs/CHOP induction and ER stress (initiated by PERK signaling) as one of the earliest event associated with UCB toxicity. However, PERK siRNA does not affected ATFs/CHOP induction by UCB while induced GCN2, suggesting a compensatory mechanism between PERK and GCN2 signaling. In conclusion, our data demonstrate that OS and ER stress are involved in UCB induced neurotoxicity in SH-SY5Y cells. The cells undergo an adaptive response against UCB induced OS and ER stress, through activation of multiple antioxidant genes (in part via Nrf2 pathway), and activation of sequential UPR sensors
XXVI Ciclo
1985
Balsiger, Alexander 1975. "The Role of cyclin O in ER stress signalling." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/565441.
Full textEn nuestro laboratorio hemos identificado recientemente un nuevo miembro de la familia de las ciclinas, la Ciclina O, la cuál puede unirse y activar a Cdk1 y Cdk2 en respuesta a estímulos apoptóticos tales como el daño genético o el estrés del retículo endoplásmico. También hemos demostrado que la Ciclina O participa en la respuesta celular desencadenada por el acúmulo de proteínas mal plegadas (UPR) actuando a través de la activación de la señalización de la ruta de PERK. El objetivo de esta tesis ha sido el estudio molecular de la participación de la Ciclina O en la respuesta al estrés del retículo. Nuestros resultados indican que los niveles de expresión de la Ciclina O incrementan en respuesta al estrés del retículo a través de rutas de la UPR que señalizan a través de la fosforilación de eIF2α y de la expresión de CHOP. Además hemos observado que en respuesta al estrés reticular la Ciclina O activa la ruta de las MAPK de manera independiente de la señalización a través de IRE1α. Este efecto posiblemente tiene lugar a través de la fosforilación y consecuente activación de MEKK4 dependiente de Cdk1 y Cdk2. Esto conlleva la activación de las kinasas de stress JNK y p38. Asimismo, mediante experimentos de fosfoproteómica hemos demostrado que un gran número de proteínas involucradas en los procesos bioquímicos de traducción y plegado dependen de la expresión de la Ciclina O.
PAGLIARINI, VITTORIA. "Apoptotic cell death modulation by ER stress and autophagy." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/202461.
Full textMularczyk, Ewa. "Understanding molecular pathology of chondrodysplasias : the role of ER stress." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/understanding-molecular-pathology-of-chondrodysplasias-the-role-of-er-stress(86ad2dcd-fcb6-4860-90d8-74f17996ac0d).html.
Full textTan, Zhijia, and 谭志佳. "Molecular analyses of chondrocyte differentiation and adaptation to ER stress." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/209435.
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Biochemistry
Doctoral
Doctor of Philosophy
Niederreiter, Lukas. "Endoplasmic reticulum (ER) stress transcription factor Xbp1 in intestinal tumourigenesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708846.
Full textElfowiris, Abdulsalam. "The regulation of gene expression in response to ER stress." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39318.
Full textLuís, Andreia Veríssimo. "Evaluation of ER stress induced by DNFB in Dendritic cells." Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/11670.
Full textA capacidade das células dendríticas (CD) em iniciar e modular respostas imunes, nomeadamente a dermatite de contacto alérgica (DCA), é fortemente dependente da sua ativação / estado de maturação. Os mecanismos moleculares pelos quais os sensibilizadores de pele induzem maturação das CD não são ainda completamente conhecidos. No entanto, foi demonstrado que sinais de perigo primários como a formação de espécies reativas de oxigénio (ERO) desempenham um importante papel neste processo. Nos últimos anos, inúmeras evidências têm estabelecido uma estreita ligação entre a produção de ERO, stresse do retículo endoplasmático (RE) e a patogénese de diversas doenças inflamatórias. Deste modo, pretendeu-se no presente trabalho avaliar a capacidade do sensibilizador cutâneo DNFB desencadear stresse do RE em CD e as concomitantes consequências na imunobiologia dessas células. Os resultados obtidos revelaram que o DNFB induz uma rápida e sustentada fosforilação do fator de iniciação de tradução eucariótico 2α (eIF2α), o aumento dos níveis proteicos do fator de transcrição ATF4 e uma modificação pós translacional na principal proteína chaperone do RE, GRP78. Verificou-se ainda que estes efeitos são dose-dependentes e parcialmente revertidos pelo antioxidante N-acetilcisteína, indicando que a alteração do estado redox celular está na origem da indução do stresse do RE observado. O tratamento das células com o chaperone químico, ácido 4-fenilbutírico (4- PBA) causou um aumento na apoptose induzida por DNFB, enquanto o prétratamento com salubrinal, um inibidor seletivo da desfosforilação de eIF2α, provocou o efeito oposto. A exacerbação pelo salubrinal da fosforilação do eIF2α induzida por DNFB causou um forte aumento da transcrição de genes de destoxificação tais como o HMOX e do gene da citoquina pró-inflamatória IL-8 tendo por sua vez o 4-PBA anulado completamente estes efeitos. Globalmente, os nossos resultados indicam que a ativação pelo DNFB do eixo eIF2α/ATF4 em CD contribui fortemente para o desenvolvimento de um microambiente pró-inflamatório e para a transcrição de genes envolvidos no restabelecimento do equilíbrio redox.
The capacity of dendritic cells (DC) to initiate and modulate immune responses, namely allergic contact dermatitis (ACD), is tightly dependent on their activation/maturation state. Molecular mechanisms driving skin sensitizersinduced DC maturation are not yet completely unrevealed, however initial danger signals such as the generation of reactive oxygen species (ROS) were shown to play an important role. In recent years innumerous evidences established a close link between ROS production, endoplasmic reticulum (ER) stress and the pathogenesis of several inflammatory diseases. Therefore, we analyzed in this work the ability of the strong sensitizer DNFB to trigger ER stress in DC and the concomitant consequences to the immunobiology of these cells. Our results revealed that DNFB induces a rapid and sustained phosphorylation of the Eukaryotic translation initiation factor 2α (eIF2α), the up regulation of ATF4 and a post translational modification at the major ER chaperone GRP78. These effects were dose dependent and partially reverted by the antioxidant N-acetylcysteine, indicating that cellular redox imbalance is in the origin of evoked ER stress. Treatment of cells with the ER chemical chaperone 4 phenylbutyric acid (4-PBA) caused an increase in DNFB-induced apoptosis while pretreatment with salubrinal, an eIF2α dephosphorylation selective inhibitor, caused the opposite effect. Exacerbation of DNFB-induced eIF2α phosphorylation by salubrinal also caused a strong increase in the transcription of detoxifying genes such as HMOX and of pro-inflammatory cytokine IL-8 while 4-PBA completely abrogated these effects. Overall, our results indicate that DNFB activation of eIF2α/ATF4 stress pathways in DC strongly contributes to generation of a pro-inflammatory microenvironment and is crucial to the transcription of genes involved in remediation of cell redox imbalance.
Monzani, Romina. "Role of ER Stress in the pathogenesis of Celiac Disease." Doctoral thesis, Università del Piemonte Orientale, 2022. http://hdl.handle.net/11579/144040.
Full textTassé, Louis-Alexandre. "The Role of Sigma-1 Receptor in Modulating Endoplasmic Reticulum Stress: Putative Relevance to Alzheimer Disease." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38395.
Full textHuang, Shirley Chien-Chieh 1978. "Control of tumor suppressor p53 by protein phosphorylation and ER stress." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78384.
Full textHühn, Martin [Verfasser]. "Endoplasmic Reticulum (ER)-stress signalling in the alveolar epithelium / Martin Hühn." Gießen : Universitätsbibliothek, 2013. http://d-nb.info/1065395310/34.
Full textMontague, K. "The role of ER stress in the pathogenesis of Kennedy's Disease." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1344063/.
Full textGkogkas, Christos G. "VAPB regulation of ER stress and its potential involvement in ALSVIII." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4305.
Full textZhu, Xiaoxi. "Intracellular localization, biochemical and biophysical properties of human Armet." Thesis, Kansas State University, 2011. http://hdl.handle.net/2097/8107.
Full textDepartment of Biochemistry
Gerald R. Reeck
Armet is a bifunctional protein widely distributed in animal species, vertebrate and invertebrate. It is an evidently part of the Unfolded Protein Response (UPR) and promotes survival in cells that are under endoplasmic-reticulum (ER) stress. It has also been found as a secreted protein with neurotrophic activity. The crystal and solution structures of human Armet show it is a helix-rich protein with two domains linked through a flexible linker region. In this study, immunofluorescence staining was used to verify Armet’s localization in ER and Golgi apparatus in MBA-MD-231 cells. Evidence for calcium binding by Armet was obtained by circular dichroism spectroscopy (the binding of calcium appeared to decrease helix content), by differential scanning calorimetry (binding of calcium resulted in a less structured protein) and two-dimensional (1H-15N HSQC) nuclear magnetic resonance spectroscopy. A difference HSQC spectrum of Armet, with and without calcium, showed peaks of increased intensity, of decreased intensity and of perturbed chemical shift. There were about 30 such peaks in total. Several of these affected amino acid residues appeared to form a cluster of negatively charged side chains that could possibly form a binding site for a calcium ion. Heterogeneity of three types was observed in recombinant Armet expressed in E. coli cells. Two bands of slightly different mobility were observed in SDS gels run in the absence of reducing agent. These may represent alternate arrangements of disulfide bonds, as previously reported by other investigators but not explained. Further, in the absence of reducing agent, a faint ladder was formed by human Armet, indicating formation of disulfides between Armet molecules. Oligomers with sedimentation coefficient greater than the monomeric protein, in the absence of reducing agent, disappeared in the presence of a reducing agent. Finally, minor species of mass differences of 98 and 180 with respect to the main protein component were observed by MALDI-TOF mass spectrometry. These studies provide a more thorough characterization of Armet than has been previously available and set the scene for future investigations of the binding of organic ligands to the protein.
Yang, Ling. "Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes." Kent State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=kent1175103480.
Full textMahmood, Ahsan. "Role of SLMAP in Endoplasmic Reticulum Stress and Unfolded Protein Response." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24399.
Full textBelahmer, Hanane [Verfasser]. "APC/C Cdh1 modulates the ER stress response via Gadd34 / Hanane Belahmer." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2011. http://d-nb.info/1021438804/34.
Full textLISTI', Angela. "UNRAVELLING THE ROLES OF THE NUCLEAR PROTEIN 1 DURING ER-STRESS INDUCTION." Doctoral thesis, Università degli Studi di Palermo, 2020. http://hdl.handle.net/10447/400605.
Full textBackground: NUPR1 was described as a transcriptional factor involved in the regulation of various cellular stress-response genes, playing a crucial role in the condition of the endoplasmic-reticulum (ER) stress, thus emerging as a common molecular factor of different pathologies, obesity, hepatic steatosis, and cancer. In the present work we aim to explore how NUPR1 interacts with some pivotal genes that are the major modulators of the ER stress and metabolic cell functions. In particular we investigated the biochemical and molecular effects arising from the loss of NUPR1 in ER stress physiological conditions. Methods: We used prolonged high fat diet (HFD) feeding to induce ER stress physiological in Nupr1+/+ and Nupr1-/- male mice compared with their respectively normal chow diet (ND) controls. We fed mice with a HFD (60% fat, 20% protein, and 20% carbohydrate) for 10 weeks to promote chronic ER stress condition (Old-HFD group, n=5). An additional group of mice (n=5) was maintained on HFD (60% fat, 20% protein, and 20% carbohydrate) for a longer duration (15 weeks) to distinguish between age-dependent and age-independent effects. Liver were collected for histological and molecular assessments. Western blots and RT-qPCR were performed to assess the expression levels of the major ER-stress response UPR-associated proteins and metabolic genes. Results: We showed the downregulation of the majority of UPR-associated proteins: BIP (p<0.0001 for protein and mRNA), ATF4 (p<0.0001 for mRNA), XBP1 (p<0.0001 for protein and mRNA), CHOP (p<0.0001 for protein and mRNA), GADD34 (p=0.0296 for mRNA) in in-vivo NUPR1-/- compared to NUPR1+/+ 10 weeks HFD mice. Western blot for the major UPR associated proteins in NURP1-/- mice at 15 weeks HFD showed similar expression trends reported at the time-point of 10 weeks. ERDj4 mRNA resulted down-regulated in NUPR1-/- compared to NUPR1+/+ 15 weeks HFD mice (p=0.0032). Among the multiple metabolic genes, we reported a down-regulation of the majority mRNA associated to lipogenesis (SREBP, ACLY, ChREBP) and lipoprotein (APOB, PPAR-alfa, MTTP) in NUPR1-/- compared to NUPR1+/ + HFD mice 15 weeks. Both LCAD and MCAD fatty acid metabolisms mRNA were also downregulated, as consequence of PPAR-alfa deficit. Similarly betaoxidation mRNA ACOX1 and CPT1-alfa, as well as MTC4 and PGK1 were downregulated in NUPR1-/- compared to NUPR1+/ + HFD mice 15 weeks. Conclusion: The results of this work confirm that NUPR1 act downstream of the PERK branch playing a crucial role of NUPR1 in the activation of UPR response in physio-pathological ER stress condition and suggest a potential contribution of NUPR1-mediated ER stress response to the development of liver steatosis.
Cooper, Angie. "Long-chain fatty acids and endoplasmic reticulum stress in pancreatic beta-cells : the role of Protein Kinase R (PKR)." Thesis, University of Plymouth, 2013. http://hdl.handle.net/10026.1/2851.
Full textCunningham, Rachael. "Investigation of Protein Targets of Pt(II) Anticancer Compounds." Thesis, University of Oregon, 2017. http://hdl.handle.net/1794/22652.
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Weichert, Nina. "Some ABCA3 mutations elevate ER stress and initiate apoptosis of lung epithelial cells." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-137380.
Full textGuo, Jinbai. "Control of cell division by nutrients, and ER stress signaling in Saccharomyces cerevisiae." Texas A&M University, 2003. http://hdl.handle.net/1969.1/5912.
Full textFang, Che. "Cytokines, alcohol metabolizing enzymes and stress-inducible ER proteins in alcoholic liver disease /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4160-2/.
Full textGwiazda, Kamila Sabina. "Role of endoplasmic reticulum calcium stores in beta-cell ER stress and lipotoxicity." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/12553.
Full textZhao, Xuechan. "An investigation into the regulation of gene expression in response to ER stress." Thesis, University of Leicester, 2014. http://hdl.handle.net/2381/29312.
Full textDarling, Nicola Jane. "Regulation of ER stress-induced cell death by the ERK1/2 signalling pathway." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708709.
Full textSmith, Jacqueline Rose. "The realities of post abortion stress syndrome." online access from Digital Dissertation Consortium, 2006. http://libweb.cityu.edu.hk/cgi-bin/er/db/ddcdiss.pl?1437842.
Full textLi, Yi. "Mechanisms of Transcriptional Regulation of Cat-1 Gene Expression by Endoplasmic Reticulum (ER) Stress." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1238790728.
Full textDI, CRISTINO FRANCESCA. "The stress-activated kinase p38MAPK contributes to ATF6 activation and resistance to ER stress in cancer cells with mutant p53." Doctoral thesis, Università degli Studi di Trieste, 2022. http://hdl.handle.net/11368/3030938.
Full textHerrenbruck, Adrienne Rose. "EFFECTS OF HIGH FAT EXPOSURE ON SKELETAL MUSCLE AUTOPHAGY AND ENDOPLASMIC RETICULUM STRESS." UKnowledge, 2018. https://uknowledge.uky.edu/khp_etds/53.
Full textSommerweiß, Dietlind. "Oleate rescues INS-1E β-cells from palmitate-induced apoptosis by preventing activation of the unfolded protein response." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-172386.
Full textPirot, Pierre. "Identification and characterization of the endoplasmic reticulum (ER)-stress pathways in pancreatic beta-cells." Doctoral thesis, Universite Libre de Bruxelles, 2007. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210623.
Full textAccumulating evidence suggest that ER stress contributes to beta-cell apoptosis in both type 1 and type 2 diabetes. Type 1 diabetes is characterized by a severe insulin deficiency resulting from chronic and progressive destruction of pancreatic beta-cells by the immune system. During this autoimmune assault, beta-cells are exposed to cytokines secreted by the immune cells infiltrating the pancreatic islets. Our group has previously shown that the pro-inflamatory cytokines interleukin-1beta (IL1-beta and interferon-gamma (IFN-gamma), via nitric oxide (NO) formation, downregulate expression and function of the ER Ca2+ pump SERCA2. This depletes beta-cell ER Ca2+ stores, leading to ER stress and apoptosis. Of note, IL1-beta alone triggers ER stress but does not induce beta-cell death, while IFN-gamma neither causes ER stress nor induces beta-cell death. Together, these cytokines cause beta-cell apoptosis but the mechanisms behind this synergistic effect were unknown.
Type 2 diabetes is characterized by both peripheral resistance to insulin, usually as a result of obesity, and deficient insulin secretion secondary to beta cell failure. Obese patients have high levels of circulating free fatty acids (FFA) and several studies have shown that the FFA palmitate induces ER stress and beta-cell apoptosis.
In the present work we initially established an experimental model to specifically activate the ER stress response in pancreatic beta-cells. For this purpose, insulinoma cells (INS-1E) or primary rat beta-cells were exposed to the reversible chemical SERCA pump blocker cyclopiazonic acid (CPA). Dose-response and time course experiments determined the best conditions to induce a marked ER stress without excessive cell death (<25%).
The first goal of the work was to understand the synergistic effects of IL1-beta and IFN-gamma leading to pancreatic beta-cell apoptosis. Our group previously observed, by microarray analysis of primary beta-cells, that IFN-gamma down-regulates mRNAs encoding for some ER chaperones. Against this background, our hypothesis was that IFN-gamma aggravates beta-cell ER stress by decreasing the ability of these cells to mount an adequate UPR. To test this hypothesis, we investigated whether IFN-gamma pre-treatment augments CPA-induced ER stress and beta cell death. The results obtained indicated that IFN-gamma pre-treatment potentiates CPA-induced apoptosis in INS-1E and primary beta-cells. This effect was specific for IFN-gamma since neither IL1-beta nor a low dose CPA pre-treatment potentiated CPA-induced apoptosis in INS-1E cells. These effects of IFN-gamma were mediated via the down regulation of genes involved in beta cell defense against ER stress, including the ER chaperones BiP, Orp150 and Grp94 as well as Sec61, a component of the ERAD pathway. This had functional consequences as evidenced by a decreased basal and CPA-induced activity of a reporter construct for the unfolded protein response element (UPRE) and augmented expression of the pro-apoptotic transcription factor Chop.
We next investigated the molecular regulation of the Chop gene in INS-1E cells in response to several pro-apoptotic and ER stress inducing agents, namely cytokines (IL1-beta and IFN-gamma), palmitate, or CPA. Detailed mutagenesis studies of the Chop promoter showed differential regulation of Chop transcription by these compounds. While cytokines (via NO production)- and palmitate-induced Chop expression was mediated via a C/EBP-ATF composite and AP-1 binding sites, CPA induction required the C/EBP-ATF site and the ER stress response element (ERSE). Cytokines, palmitate and CPA induced ATF4 protein expression and further binding to the C/EBP-ATF composite site, as shown by Western blot and EMSA experiments. There was also formation of distinct AP-1 dimers and binding to the AP-1 site after exposure to cytokines or palmitate.
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Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished
Pei, Lim-cho Steven, and 貝念祖. "Role(s) of p53/p63 in chondrocyte re-differentiation upon activation of ER stress." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/198926.
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Biochemistry
Master
Master of Philosophy
DI, GIACOMO GIUSEPPINA. "Role of Transglutaminase 2 in immunogenic and ER-stress induced cell death in cancer." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/202267.
Full textLENNA, STEFANIA. "ROLE OF HLA-B35 AND ER STRESS IN SCLERODERMA PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/215411.
Full textMullan, Lorna A. "Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/stimulation-of-intracellular-proteolytic-degradation-as-a-means-of-reducing-er-stress-in-a-model-of-skeletal-dysplasia(b2bb722a-4c5b-4cae-8624-c83aeddd3d2a).html.
Full textIde, Yuya. "Cardio-protective effects of VCP modulator KUS121 in murine and porcine models of myocardial infarction." Kyoto University, 2020. http://hdl.handle.net/2433/253150.
Full textSte-Marie, Chantal. "Anxiety and social stress related to adolescent gambling behavior." Thesis, online access from Digital Dissertation Consortium access full-text, 2001. http://libweb.cityu.edu.hk/cgi-bin/er/db/ddcdiss.pl?MQ75257.
Full textCasas, Prat María. "CPT1C-dependent regulation of GluA1 trafficking under metabolic stress." Doctoral thesis, Universitat Internacional de Catalunya, 2019. http://hdl.handle.net/10803/668107.
Full textMcDermott, Benjamin Thomas. "Investigation into the role of ER stress in the pathology of metaphyseal chondrodysplasia type Schmid." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501983.
Full textHinte, Florian [Verfasser], and Wolfram [Akademischer Betreuer] Brune. "Interaktion des Cytomegalovirus mit dem IRE1-abhängigen ER-Stress-Signalweg / Florian Hinte ; Betreuer: Wolfram Brune." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2020. http://d-nb.info/1216629390/34.
Full textOslowski, Christine M. "TXNIP is a Mediator of ER Stress-Induced β-Cell Inflammation and Apoptosis: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/611.
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