Gotowe bibliografie tematyczne / ER stress

Gotowa bibliografia na temat „ER stress”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 lipca 2024

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Artykuły w czasopismach na temat "ER stress"

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Jaenicke, Lothar. "ER-Stress". Chemie in unserer Zeit 40, nr 3 (czerwiec 2006): 161. http://dx.doi.org/10.1002/ciuz.200690036.

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Zito, Ester. "Targeting ER stress/ER stress response in myopathies". Redox Biology 26 (wrzesień 2019): 101232. http://dx.doi.org/10.1016/j.redox.2019.101232.

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Kumar, Vaishali, i Shuvadeep Maity. "ER Stress-Sensor Proteins and ER-Mitochondrial Crosstalk—Signaling Beyond (ER) Stress Response". Biomolecules 11, nr 2 (28.01.2021): 173. http://dx.doi.org/10.3390/biom11020173.

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Recent studies undoubtedly show the importance of inter organellar connections to maintain cellular homeostasis. In normal physiological conditions or in the presence of cellular and environmental stress, each organelle responds alone or in coordination to maintain cellular function. The Endoplasmic reticulum (ER) and mitochondria are two important organelles with very specialized structural and functional properties. These two organelles are physically connected through very specialized proteins in the region called the mitochondria-associated ER membrane (MAM). The molecular foundation of this relationship is complex and involves not only ion homeostasis through the shuttling of calcium but also many structural and apoptotic proteins. IRE1alpha and PERK are known for their canonical function as an ER stress sensor controlling unfolded protein response during ER stress. The presence of these transmembrane proteins at the MAM indicates its potential involvement in other biological functions beyond ER stress signaling. Many recent studies have now focused on the non-canonical function of these sensors. In this review, we will focus on ER mitochondrial interdependence with special emphasis on the non-canonical role of ER stress sensors beyond ER stress.
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Kawaguchi, S., i D. T. W. Ng. "Sensing ER Stress". Science 333, nr 6051 (29.09.2011): 1830–31. http://dx.doi.org/10.1126/science.1212840.

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Gough, N. R. "Neuronal ER Stress". Science Signaling 3, nr 152 (14.12.2010): ec378-ec378. http://dx.doi.org/10.1126/scisignal.3152ec378.

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Vincenz, Lisa, i F. Ulrich Hartl. "Sugarcoating ER Stress". Cell 156, nr 6 (marzec 2014): 1125–27. http://dx.doi.org/10.1016/j.cell.2014.02.035.

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Mateus, Duarte, Elettra Sara Marini, Cinzia Progida i Oddmund Bakke. "Rab7a modulates ER stress and ER morphology". Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1865, nr 5 (maj 2018): 781–93. http://dx.doi.org/10.1016/j.bbamcr.2018.02.011.

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Gorman, Adrienne M., Sandra J. M. Healy, Richard Jäger i Afshin Samali. "Stress management at the ER: Regulators of ER stress-induced apoptosis". Pharmacology & Therapeutics 134, nr 3 (czerwiec 2012): 306–16. http://dx.doi.org/10.1016/j.pharmthera.2012.02.003.

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Begum, Gulnaz, Lloyd Harvey, C. Edward Dixon i Dandan Sun. "ER Stress and Effects of DHA as an ER Stress Inhibitor". Translational Stroke Research 4, nr 6 (20.08.2013): 635–42. http://dx.doi.org/10.1007/s12975-013-0282-1.

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Lee, Amy S., i Linda M. Hendershot. "ER stress and cancer". Cancer Biology & Therapy 5, nr 7 (lipiec 2006): 721–22. http://dx.doi.org/10.4161/cbt.5.7.3120.

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Rozprawy doktorskie na temat "ER stress"

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Chan, Cheuk-wing Wilson, i 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.

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

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Lo, 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.

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Lo, Ling-kit Rebecca, i 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.

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Adolph, 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.

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Alves, Inês Sofia Moutinho. "Contribution of ER stress to tumor immunosuppressive microenvironment". Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/14290.

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Mestrado em Bioquímica - Bioquímica Clínica
Breast 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.
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Narayanan, Siddharth. "Crosstalk between the ER stress pathway and osmotic stress in S. cerevisiae". Thesis, Durham University, 2011. http://etheses.dur.ac.uk/3435/.

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In Saccharomyces cerevisiae, the general stress response (GSR) protects cells from diverse stress conditions such as osmotic stress and heat stress, while the Unfolded Protein Response (UPR) is a protein folding stress signalling pathway which maintains homeostasis of the endoplasmic reticulum (ER). A mechanism of how and if at all the UPR integrates with other pathways is largely unknown. The focus of this thesis was to determine whether essential components of the UPR like the bZIP transcription factor Hac1p and the Rpd3p-Sin3p histone deacetylase integrated within osmotic stress and to identify a possible mechanism of such an integration event. Data from this thesis demonstrate that UPR components protect cells from hyperosmotic stress. Hac1p is a direct positive regulator of GSR genes. Rpd3p and Hac1p belong to the same pathway in activating GSR genes. Data also suggest that Hac1p does not contribute to the increase in nucleosomal histone acetylation levels after osmotic stress. The Gcn5 histone acetyltransferase contributes to the increase in histone acetylation observed after osmotic stress. The Rpd3p represses GSR genes in unstressed cells but also contributes to the activation of GSR genes after hyperosmotic shock. The Rpd3 large complex and not the small complex is involved regulating GSR gene expression. Subsequent investigation demonstrates that a possible mechanism by which the UPR contributes to the GSR gene activation is by the RNA polymerase II clearance at the GSR gene promoters.
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Qaisiya, 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.

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2012/2013
Elevati 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
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Balsiger, Alexander 1975. "The Role of cyclin O in ER stress signalling". Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/565441.

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We recently identified a novel cyclin called Cyclin O which is able to bind and activate Cdk1 and Cdk2 in response to intrinsic apoptotic stimuli like DNA damage or ER stress. Cyclin O has been shown to be involved in the unfolded protein response (UPR) as an activator of PERK signalling. The aim of this thesis has been to study the molecular role of Cyclin O in response to ER stress. We have found that expression of Cyclin O is upregulated upon ER stress by pathways of the UPR that signal through eIF2α phosphorylation and CHOP expression. Furthermore, we have observed that Cyclin O activates the MAPK pathways independently of IRE1α signalling. This effect is most likely mediated by Cdk1 and Cdk2-dependent phosphorylation and consequent activation of MEKK4, which leads to the activation of JNK and p38. We have also found employing phosphoproteomics technology that many proteins involved in protein folding and translation depend on Cyclin O.
En 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.
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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.

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Cancer is a highly complex disease which is caused by an upset of balance between cell growth and death. During cell transformation, abnormality in the machinery of apoptosis often occurs, resulting in a chemotherapy-resistant phenotype of cancerous cells. Endoplasmic reticulum stress (ER stress) and autophagic process are now representing serious candidates as alternative pathways to induce cell death in chemotherapy-resistant tumor cells. If on the one hand they induce cytoprotective functions to reestablish normal cellular homeostasis, on the other hand they contribute to an efficient cell killing when the stress is prolonged and unresolved. Therefore, harnessing stress-induced survival response, such as ER stress and autophagy, may represent a new anticancer strategy to induce cell death in apoptosis-resistant tumors. In line with this hypothesis, it has been recently shown that some chemotherapeutic agents overcome apoptosis-resistance through induction of both autophagy and ER stress. Thus, understanding the link between ER stress/apoptosis and autophagy/apoptosis induction may offer the opportunity to find out new targets to design more effective therapeutic regimes to treat cancer malignancies. Here, we show that: i) the down-regulation of the transcription factor E2F1, a key regulator of proliferation and cell death, represents a critical event in ER stress-induced apoptosis, unveiling E2F1 inactivation as a novel therapeutic strategy to increase the response of tumor cells to ER stress based anticancer treatments; ii) oncogenic activating mutation in B-RAF confers resistance to autophagy in response to both classical inducers (serum starvation and rapamycin), and to ER stress-induced apoptosis (fenretinide and velcade), suggesting that autophagy is required for efficient melanoma cell killing; iii) Ambra1, an essential regulator of autophagy, plays a role in the regulation of apoptosis, and consequently in the interplay between autophagy and apoptosis, underlining the functional link existing between these processes.
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Książki na temat "ER stress"

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Garcia, Enrique Jose. ER stress and lipid droplet-dependent proteostasis in response to lipid stress in yeast and a novel congenital muscular dystrophy. [New York, N.Y.?]: [publisher not identified], 2019.

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ER for the soul: Veterans' stories of hope and healing. Auburn, CA: Six Wings and a Prayer Productions, 2012.

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Gerald, Lewis, Blunt Grace L, Durso Carmen L i Massachusetts Continuing Legal Education, Inc. (1982- ), red. Proving or protecting against "intangible harm": A new(er) understanding of psychological damage. [Boston, Mass.]: MCLE, 2004.

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Er se bu xue cao nai yan ji li ji nai yan ji yin gong neng fen xi. Beijing: Ke xue chu ban she, 2013.

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Toda, Katsuyuki. Xuan feng bang qiu er. Taibei Shi: Dong li chu ban she, 1997.

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Shanghai hua tu tu dou wen hua chuan bo you xian gong si, red. Shuang chong xiong er. Hangzhou: Zhejiang shao nian er tong chu ban she, 2015.

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Hiruta, Tatsuya. Xin gong fu xuan feng er. Taibei Shi: Dong li chu ban she you xian gong si, 2000.

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Hiruta, Tatsuya. Xin gong fu xuan feng er. Taibei Shi: Dong li chu ban she you xian gong si, 1997.

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Hiruta, Tatsuya. Xin gong fu xuan feng er. Taibei Shi: Dong li chu ban she you xian gong si, 1999.

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Hiruta, Tatsuya. Xin gong fu xuan feng er. Taibei Shi: Dong li chu ban she you xian gong si, 1996.

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Części książek na temat "ER stress"

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Shimazawa, Masamitsu, i Hideaki Hara. "ER Stress". W Neuroprotection and Neuroregeneration for Retinal Diseases, 67–83. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54965-9_5.

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Howell, Stephen. "Cytoplasm: ER Stress". W Molecular Biology, 1–25. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0263-7_9-1.

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Garg, Abhishek D., Agnieszka Kaczmarek, Dmitri V. Krysko i Peter Vandenabeele. "ER Stress and Inflammation". W Endoplasmic Reticulum Stress in Health and Disease, 257–79. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9_11.

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Howell, Stephen. "ER Stress Signaling in Plants". W Molecular Biology, 213–43. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7570-5_9.

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Vervliet, Tim, Santeri Kiviluoto i Geert Bultynck. "ER Stress and UPR Through Dysregulated ER Ca2+ Homeostasis and Signaling". W Endoplasmic Reticulum Stress in Health and Disease, 107–42. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9_5.

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Ji, Cheng, i Neil Kaplowitz. "ER Stress Signaling in Hepatic Injury". W Signaling Pathways in Liver Diseases, 287–304. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00150-5_19.

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van Vliet, Alexander R., i Patrizia Agostinis. "Mitochondria-Associated Membranes and ER Stress". W Current Topics in Microbiology and Immunology, 73–102. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/82_2017_2.

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Tomczak, Michal F., Arthur Kaser i Richard S. Blumberg. "ER Stress in Intestinal Inflammatory Disease". W Endoplasmic Reticulum Stress in Health and Disease, 281–98. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9_12.

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Urano, Fumihiko, i Bryan O’Sullivan-Murphy. "Pathological ER Stress in β Cells". W Endoplasmic Reticulum Stress in Health and Disease, 215–30. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9_9.

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Verkuil, Bart, i Arnold van Emmerik. "Wat is er met me aan de hand?" W Omgaan met stress en burnout, 11–28. Houten: Bohn Stafleu van Loghum, 2007. http://dx.doi.org/10.1007/978-90-313-6415-2_1.

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Streszczenia konferencji na temat "ER stress"

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Tsukiji, Tetsuhiro, Shigeaki Saito, Yoshinobu Asako i Toshihiro Kawakami. "Shear Stress of ER Suspensions". W ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0459.

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Abstract The shear stresses of ER (Electro-rheological) suspensions are measured by changing a shear rate, amplitude and frequency of electric fields using rotational viscometer whose gap between electrodes can be changed. We use two ER suspensions which are called ERFC and ERFP. ERFC consist of cellulose suspended in silicone oil. The size of cellulose particles is typically about 10∼20 μm and a viscosity of silicone oil is 10mm2/s. Cellulose concentration is 20wt.% and the percentage of moisture content is 0.6%. ERFP contains highly sulfonated poly (styrene-co-divinylbenzene) particles. An average particle diameter of ERFP is 9 microns and the water content is 2.0 wt.%. Unipolar sine-wave electric fields which is AC with DC bias and bipolar sine-wave electric fields without DC bias are used. The shear rates of 400 s−1 are employed. Amplitudes of the electric fields are 0.4 and 0.8 kV/mm and DC component is 1.0 kV/mm for unipolar sine-wave electric fields. Amplitudes are between 1.0 and 2.5 kV/mm for bipolar sine-wave electric fields. The frequency of the electric fields is changed from 0.1 to 100 Hz. Dependence of the shear stress on electrical excitation frequency is investigared.
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Corral, Gonzalo, i Andrew J. Whittle. "Re-Analysis of Deep Excavation Collapse Using a Generalized Effective Stress Soil Model". W Earth Retention Conference (ER) 2010. Reston, VA: American Society of Civil Engineers, 2010. http://dx.doi.org/10.1061/41128(384)72.

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Gewandter, JS, i MA O'Reilly. "Loss of the ER Stress Sensor Protein, BiP, in Hyperoxia Does Not Activate the Classic ER Stress Response." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4183.

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Gong, Haijun, i Lu Feng. "Probabilistic verification of ER stress-induced signaling pathways". W 2014 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2014. http://dx.doi.org/10.1109/bibm.2014.6999149.

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Wang, Yixuan, Jinrui Huang i Siqi Xiong. "Relations between ER Stress, UPR and Cancer Biology". W 2021 International Conference on Public Art and Human Development ( ICPAHD 2021). Paris, France: Atlantis Press, 2022. http://dx.doi.org/10.2991/assehr.k.220110.056.

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Tsukiji, Tetsuhiro, i Shinsuke Tanabe. "ER Effect in Liquid Crystal". W ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-1943.

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Abstract Liquid crystal is one of homogeneous ER (Electro-rheological) fluids in some range of temperature. In the present study the effect of electric fields on shear stress in liquid crystal is investigated using rotational viscometer. The shear stresses are measured by changing a shear rate, amplitude and frequency of electric fields. Dependence of the shear stress on electrical excitation frequency is mainly investigated. Furthermore flow visualization is conducted and relation between flow rate and pressure drop is measured when liquid crystal flows between two parallel-plate electrodes under application of electric fields. The experimental results are compared with previous ones for ER suspensions.
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Abdelsalam, Shahenda Salaheldine, i Abdelali Agouni. "Protein Tyrosine Phosphatase (PTP) 1B Inhibition Improves Endoplasmic Reticulum Stress-Induced Apoptosis and Impaired Angiogenic Response in Endothelial Cells". W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0110.

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Insulin is not only important for glucose homeostasis, but also plays a critical role in the activation of endothelial nitric oxide synthase (eNOS) to synthesize nitric oxide (NO) and keeping the endothelium functional. Conditions which result in insulin resistance, such as diabetes and obesity, cause impairment of endothelial function, a condition known as endothelial dysfunction that features a reduced release of NO. Protein tyrosine phosphatase (PTP) 1B, is a known negative regulator of insulin receptor, that has been implicated in the pathogenesis of insulin resistance and endothelial dysfunction. Owing to its critical location at the surface of the endoplasmic reticulum (ER), PTP1B has been found to play an important role in ER stress response. However, the role of ER stress in PTP1B-mediated endothelial dysfunction is not fully elucidated. Toa address this, ER stress was induced pharmacologically in endothelial cells using thapsigargin, in the presence or absence of either a small molecule inhibitor of PTP1B or silencing siRNA duplexes, followed by the assessment of the expression of key ER stress markers, angiogenic capacity and apoptotic signals. We report here, that PTP1B inhibition protected cells against ER stress and ER stress-induced impairment in eNOS activation and angiogenic capacity. PTP1B inhibition or silencing also protected against ER stress-induced endothelial cell apoptosis. Moreover, PTP1B blockade also suppressed ER stress-activated autophagy. Our data emphasize on the critical role of PTP1B in ER stress-mediated endothelial cell dysfunction and highlights the therapeutic potential of PTP1B inhibition against ER stress-mediated cell death and impairment of endothelial function to prevent cardiovascular disease in pathologies charactereized by the activation of ER stress such as diabetes.
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FILISKO, F. E. "ALTERNATIVE VIEW FOR YIELD STRESS OF ER/MR MATERIALS". W Proceedings of the 10th International Conference on ERMR 2006. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812771209_0010.

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Tsukiji, Tetsuhiro, i Norihiko Tanaka. "Effects of Electrical Change on the Shear Stress in ER Fluids (Frequency Response)". W ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-0252.

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Abstract The frequency response of ER fluids in steady shear to sine-wave changes in the applied electric field is investigated. The ER fluids used in the present study consist of cellulose suspended in silicone oil. The size of cellulose particles is typically about 10∼20μm and a viscosity of silicone oil is 10mm2/s. Cellulose concentration is 20 wt. % and the percentage of moisture content is 0.6 %. Unipolar wave electric fields are used and the shear rates of 120 s−1, 400 s−1 are employed. Amplitudes of the electric fields are 0.1 and 0.4 kV/mm and DC component is 0.5 kV/mm. The frequency of the electric fields is changed from 0.1 to 1000 Hz. The rheological properties of ER fluids are carried out using rotational viscometer which is improved to apply the electric field on the ER fluids. The central value, the amplitude and the phase angle of the shear stress are measured. Dependence of the shear stress on electrical excitation frequency is investigated.
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Urbina, Cristina, Silvia De la Flor, Francesc Gispert-Guirado i Francesc Ferrando. "New Interpretation of the Electrical Resistivity Measurements for Obtaining NiTi SMA Stress-Free Transformation Temperatures". W ASME 2012 11th Biennial Conference on Engineering Systems Design and Analysis. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/esda2012-82256.

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The objective of this study is to clarify and to improve the interpretation of the ER measurements used to obtain NiTi SMA stress-free transformation temperatures for the austenite to martensite transformation process. To achieve this objective, the transformation temperatures of NiTi SMA wires are measured by ER using the Ling and Kaplow interpretation and are compared and complemented by weight fraction diagrams. The weight fractions are obtained from XRD profiles using the Parametric Rietveld refinement and adequate software. As a result of comparing both techniques, a new interpretation of the ER curves is proposed. This new interpretation is based on the shape of NiTi ER curve, which depends on the quantity of R-phase in the NiTi SMA. The quantity of the R-phase is obtained by weight fraction diagrams. According to the findings presented here, a new criterion for R-phase and martensite transformation temperatures is proposed.
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Raporty organizacyjne na temat "ER stress"

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Hoang, Sony. -Synuclein and Mitochondrial Dysfunction Induced ER Stress Leading to Parkinson’s Disease. Ames (Iowa): Iowa State University, styczeń 2020. http://dx.doi.org/10.31274/cc-20240624-857.

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Zanetti, Maurizio, Kevin Chiu i Jeffrey Rodvold. On the Origin of Prostate Cancer Stem Cells through Transmissible ER Stress-Mediated Epithelial to Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2013. http://dx.doi.org/10.21236/ada580103.

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Zanetti, Maurizio, Keivn Chiu, Jeffrey Rodvold i Maurizio Zanetti. On the Origin of Prostate Cancer Stem Cells through Transmissible ER Stress-Mediated Epithelial to Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada591354.

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