Gotowe bibliografie tematyczne / Endoplasmic reticulum stress

Spis treści

  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
  6. Raporty organizacyjne

Gotowa bibliografia na temat „Endoplasmic reticulum stress”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 25 lipca 2025

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Artykuły w czasopismach na temat "Endoplasmic reticulum stress"

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BANHEGYI, G., P. BAUMEISTER, A. BENEDETTI, et al. "Endoplasmic Reticulum Stress." Annals of the New York Academy of Sciences 1113, no. 1 (2007): 58–71. http://dx.doi.org/10.1196/annals.1391.007.

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Schröder, M. "Endoplasmic reticulum stress responses." Cellular and Molecular Life Sciences 65, no. 6 (2007): 862–94. http://dx.doi.org/10.1007/s00018-007-7383-5.

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Hu, Yanan, Wenhao Yang, Liang Xie, Tao Liu, Hanmin Liu, and Bin Liu. "Endoplasmic reticulum stress and pulmonary hypertension." Pulmonary Circulation 10, no. 1 (2020): 204589401990012. http://dx.doi.org/10.1177/2045894019900121.

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Pulmonary hypertension is a fatal disease of which pulmonary vasculopathy is the main pathological feature resulting in the mean pulmonary arterial pressure higher than 25 mmHg. Moreover, pulmonary hypertension remains a tough problem with unclear molecular mechanisms. There have been dozens of studies about endoplasmic reticulum stress during the onset of pulmonary hypertension in patients, suggesting that endoplasmic reticulum stress may have a critical effect on the pathogenesis of pulmonary hypertension. The review aims to summarize the rationale to elucidate the role of endoplasmic reticu
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Koch, G., M. Smith, D. Macer, P. Webster, and R. Mortara. "Endoplasmic reticulum contains a common, abundant calcium-binding glycoprotein, endoplasmin." Journal of Cell Science 86, no. 1 (1986): 217–32. http://dx.doi.org/10.1242/jcs.86.1.217.

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The most abundant protein in microsomal membrane preparations from mammalian cells has been identified as a 100 X 10(3) Mr concanavalin A-binding glycoprotein. The glycosyl moiety of the glycoprotein is completely sensitive to endoglycosidase H, suggesting a predominantly endoplasmic reticulum localization in the cell. Using a monospecific antibody it was shown by binding and immunofluorescence studies that the glycoprotein is intracellular. Immunoelectron microscopy showed that the glycoprotein was at least 100 times more concentrated in the endoplasmic reticulum than in any other cellular or
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Das, Swapan K., Winston S. Chu, Ashis K. Mondal, et al. "Effect of pioglitazone treatment on endoplasmic reticulum stress response in human adipose and in palmitate-induced stress in human liver and adipose cell lines." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (2008): E393—E400. http://dx.doi.org/10.1152/ajpendo.90355.2008.

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Obesity and elevated cytokine secretion result in a chronic inflammatory state and may cause the insulin resistance observed in type 2 diabetes. Recent studies suggest a key role for endoplasmic reticulum stress in hepatocytes and adipocytes from obese mice, resulting in reduced insulin sensitivity. To address the hypothesis that thiazolidinediones, which improve peripheral insulin sensitivity, act in part by reducing the endoplasmic reticulum stress response, we tested subcutaneous adipose tissue from 20 obese volunteers treated with pioglitazone for 10 wk. We also experimentally induced endo
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Groenendyk, Jody, Xiao Fan, Zhenling Peng, Lukasz Kurgan, and Marek Michalak. "Endoplasmic reticulum and the microRNA environment in the cardiovascular system." Canadian Journal of Physiology and Pharmacology 97, no. 6 (2019): 515–27. http://dx.doi.org/10.1139/cjpp-2018-0720.

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Stress responses are important to human physiology and pathology, and the inability to adapt to cellular stress leads to cell death. To mitigate cellular stress and re-establish homeostasis, cells, including those in the cardiovascular system, activate stress coping response mechanisms. The endoplasmic reticulum, a component of the cellular reticular network in cardiac cells, mobilizes so-called endoplasmic reticulum stress coping responses, such as the unfolded protein response. MicroRNAs play an important part in the maintenance of cellular and tissue homeostasis, perform a central role in t
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Hadley, Gina, Ain A. Neuhaus, Yvonne Couch, et al. "The role of the endoplasmic reticulum stress response following cerebral ischemia." International Journal of Stroke 13, no. 4 (2017): 379–90. http://dx.doi.org/10.1177/1747493017724584.

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Background Cornu ammonis 3 (CA3) hippocampal neurons are resistant to global ischemia, whereas cornu ammonis (CA1) 1 neurons are vulnerable. Hamartin expression in CA3 neurons mediates this endogenous resistance via productive autophagy. Neurons lacking hamartin demonstrate exacerbated endoplasmic reticulum stress and increased cell death. We investigated endoplasmic reticulum stress responses in CA1 and CA3 regions following global cerebral ischemia, and whether pharmacological modulation of endoplasmic reticulum stress or autophagy altered neuronal viability . Methods In vivo: male Wistar ra
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HAN, Sevtap, Mecit Orhan ULUDAĞ, and Emine DEMİREL YILMAZ. "Endoplasmic Reticulum Stress and Hypertension." Turkiye Klinikleri Journal of Internal Medicine 4, no. 3 (2019): 147–53. http://dx.doi.org/10.5336/intermed.2019-65618.

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Martinez, Alexis, Cristian M. Lamaizon, Cristian Valls, et al. "c-Abl Phosphorylates MFN2 to Regulate Mitochondrial Morphology in Cells under Endoplasmic Reticulum and Oxidative Stress, Impacting Cell Survival and Neurodegeneration." Antioxidants 12, no. 11 (2023): 2007. http://dx.doi.org/10.3390/antiox12112007.

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The endoplasmic reticulum is a subcellular organelle key in the control of synthesis, folding, and sorting of proteins. Under endoplasmic reticulum stress, an adaptative unfolded protein response is activated; however, if this activation is prolonged, cells can undergo cell death, in part due to oxidative stress and mitochondrial fragmentation. Here, we report that endoplasmic reticulum stress activates c-Abl tyrosine kinase, inducing its translocation to mitochondria. We found that endoplasmic reticulum stress-activated c-Abl interacts with and phosphorylates the mitochondrial fusion protein
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Li, Yina, Mingyang Li, Shi Feng, et al. "Ferroptosis and endoplasmic reticulum stress in ischemic stroke." Neural Regeneration Research 19, no. 3 (2023): 611–18. http://dx.doi.org/10.4103/1673-5374.380870.

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Abstract Ferroptosis is a form of non-apoptotic programmed cell death, and its mechanisms mainly involve the accumulation of lipid peroxides, imbalance in the amino acid antioxidant system, and disordered iron metabolism. The primary organelle responsible for coordinating external challenges and internal cell demands is the endoplasmic reticulum, and the progression of inflammatory diseases can trigger endoplasmic reticulum stress. Evidence has suggested that ferroptosis may share pathways or interact with endoplasmic reticulum stress in many diseases and plays a role in cell survival. Ferropt
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Rozprawy doktorskie na temat "Endoplasmic reticulum stress"

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

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Mammalian/mechanistic target of mTOR complex 1 (mTORC1) regulates multiple cellular processes, including de novo protein synthesis, autophagy and apoptosis. mTORC1 overactivation occurs in a range of cancers and benign tumour dispositions as a result of mutations which increase mitogenic stimulus or cause malfunction of the tuberous sclerosis complex, the prime regulator of mTORC1 activity. mTORC1 overactivation results in elevated endoplasmic reticulum (ER) stress which, at low levels, elicits a pro-survival response. However, prolonged or excessive ER stress causes cell death. The present st
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Zachariah, Matshediso. "High selenium induces endothelial dysfunction via endoplasmic reticulum stress." Thesis, University of Surrey, 2017. http://epubs.surrey.ac.uk/845246/.

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Selenium (Se) is associated with insulin resistance and may affect endothelial function thereby increasing the risk of type 2 diabetes and associated cardiovascular disease (CVD). However, the molecular mechanisms involved are not clear. The endoplasmic-reticulum (ER) stress response is a mechanism involved in apoptosis induced by high Se in some cancer cells and, also in the pathogenesis of insulin resistance and endothelial dysfunction (ED). Thus, we hypothesised that high Se status causes ED through ER stress response. Endothelial cells (HUVECs) and EA.hy926 cell lines were treated with sel
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Voyias, Philip D. "Regulation of endoplasmic reticulum stress in adipose tissue metabolism." Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/74256/.

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Obesity is the most significant risk factor for developing type II diabetes mellitus (T2DM). Obesity induces adipocyte endoplasmic reticulum (ER) stress, prior to onset of insulin resistance. A pathological inability of white adipose tissue (WAT) to expand to accommodate excess energy is predominantly due to impaired adipogenesis. The research hypothesis was that ER stress in human WAT is important in inducing WAT dysfunction and subsequent insulin resistance and T2DM. The aims of this study were to elucidate interactions of ER stress in human WAT and to characterise the role of ER stress in h
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Furmanik, Malgorzata. "The role of endoplasmic reticulum stress in vascular calcification." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-endoplasmic-reticulum-stress-in-vascular-calcification(a0138614-e3d8-42ef-9cbf-02a01f6e6eaf).html.

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Vascular calcification (VC) is a health problem common in ageing populations, diabetes and chronic kidney disease. It leads to vascular stiffening and heart failure. VC is a regulated process mediated by vascular smooth muscle cells (VSMCs), with similarities to developmental osteogenesis. The exact molecular events responsible for triggering it are unknown. The endoplasmic reticulum (ER) is involved in folding of proteins. ER stress occurs as a result of unfolded protein accumulation and has been implicated in osteoblast differentiation and bone mineralization. Therefore, I hypothesized that
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Darling, Nicola Jane. "Regulation of ER stress-induced cell death by the ERK1/2 signalling pathway." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708709.

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

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Endoplasmic reticulum (ER) stress plays an important role in the pathogenesis of obesity-related inflammation and insulin resistance in adipose tissue. However, the mechanisms responsible for induction of ER stress are presently unclear. Proper ER redox state is crucial for oxidative protein folding and secretion and impaired protein folding in ER leads to induction of unfolded protein response and ER stress. However, while ER redox state is more oxidizing compared to the rest of the cell, its regulation is poorly understood. In order to determine the effects of ER redox state on development o
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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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Preston, Amanda Miriam Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "The role of endoplasmic reticulum stress in beta-cell lipoapoptosis." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41231.

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Beta-cell failure is a key step in the progression from metabolic disorder to overt type 2 diabetes (T2D). This failure is characterised by both secretory defects and loss of beta-cell mass, the latter most likely through increases in the rate of apoptosis. Although the mechanisms underlying these beta-cell defects are unclear, evidence suggests that chronic exposure of beta-cells to elevated fatty acid (FA) plays a role in disease development in genetically susceptible individuals. Furthermore, it has been postulated that endoplasmic reticulum (ER) stress signalling pathways (the unfolded pro
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Katsoulieris, Elias. "Oxidatives and Endoplasmic Reticulum Stress in Kidney Priximal Tubule Cells." Thesis, University of Brighton, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506517.

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

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Książki na temat "Endoplasmic reticulum stress"

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Agostinis, Patrizia, and Samali Afshin, eds. Endoplasmic Reticulum Stress in Health and Disease. Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9.

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Wagner, Cameron. Endoplasmic Reticulum Stress: Regulation, Function and Role in Health and Disease. Nova Science Publishers, Incorporated, 2016.

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Zhang, Kezhong, ed. Endoplasmic Reticulum Stress Response and Transcriptional Reprogramming. Frontiers SA Media, 2015. http://dx.doi.org/10.3389/978-2-88919-436-0.

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Agostinis, Patrizia, and Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer Netherlands, 2014.

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Agostinis, Patrizia, and Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer London, Limited, 2012.

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Endoplasmic Reticulum Stress In Health And Disease. Springer, 2012.

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Schäfer, Patrick, Lorenzo Frigerio, Federica Brandizzi, and Stephen H. Howell, eds. Endoplasmic reticulum - shape and function in stress translation. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-344-8.

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So, Jonathan. Characterization of the endoplasmic reticulum stress response in bipolar-I disorder. 2006.

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Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier, 2020. http://dx.doi.org/10.1016/c2019-0-04102-7.

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Madkour, Loutfy H. Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier Science & Technology Books, 2020.

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Części książek na temat "Endoplasmic reticulum stress"

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van Vliet, Alex, and Patrizia Agostinis. "Endoplasmic Reticulum Stress." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_1888-2.

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van Vliet, Alex, and Patrizia Agostinis. "Endoplasmic Reticulum Stress." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_1888.

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Agostinis, Patrizia. "Endoplasmic Reticulum Stress." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1888.

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Parmar, Vipul M., and Martin Schröder. "Sensing Endoplasmic Reticulum Stress." In Advances in Experimental Medicine and Biology. Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-1680-7_10.

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Qi, Zhihao, and Linxi Chen. "Endoplasmic Reticulum Stress and Autophagy." In Autophagy: Biology and Diseases. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0602-4_8.

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Kaser, Arthur. "Autophagy and Endoplasmic Reticulum Stress." In Crohn's Disease and Ulcerative Colitis. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33703-6_12.

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Yilmaz, Erkan. "Endoplasmic Reticulum Stress and Obesity." In Obesity and Lipotoxicity. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48382-5_11.

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Xu, Hui, Feng-Yang Guo, and Zhong-Yuan Zhang. "Alteration of Endoplasmic Reticulum Stress." In Coal-burning Type of Endemic Fluorosis. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1498-9_16.

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Yilmaz, Erkan. "Endoplasmic Reticulum Stress and Obesity." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-63657-8_13.

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Healy, Sandra JM, Tom Verfaillie, Richard Jäger, Patrizia Agostinis, and Afshin Samali. "Biology of the Endoplasmic Reticulum." In Endoplasmic Reticulum Stress in Health and Disease. Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9_1.

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Streszczenia konferencji na temat "Endoplasmic reticulum stress"

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Ponomareva, A. A., S. A. Dmitrieva, and F. V. Minibaeva. "Endoplasmic reticulum: stress from stress." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-361.

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Song, Yue, Yueqi Wang, and Yikai Jiang. "Endoplasmic reticulum stress and related diseases." In Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), edited by Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3021655.

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O’reilly, S. "P105 Endoplasmic reticulum stress mediates dermal fibrosis." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.121.

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O’reilly, S. "AB0196 Endoplasmic reticulum stress in systemic sclerosis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6443.

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Hassan, Ihab, Michael S. Zhang, Linda S. Powers, Kevin L. Legge, and Martha M. Monick. "Influenza A Infection Modulates Endoplasmic Reticulum Stress." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1805.

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Ma, X., E. Dobrinskikh, J. S. Kurche, et al. "Endoplasmic Reticulum Stress in MUC5B-Driven Lung Fibrosis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4216.

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Delbrel, E., P. S. Fenwick, C. Wrench, J. R. Baker, L. E. Donnelly, and P. J. Barnes. "Endoplasmic reticulum stress implication in fibroblast senescence in COPD." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.97.

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Chen, Haoyi. "Review on the Endoplasmic Reticulum Stress and Related Diseases." In IMIP '21: 2021 3rd International Conference on Intelligent Medicine and Image Processing. ACM, 2021. http://dx.doi.org/10.1145/3468945.3468972.

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Kim, So Ri, Dong Im Kim, Seung Yong Park, et al. "The Role Of Endoplasmic Reticulum Stress In Bronchial Asthma." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5635.

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Degryse, Amber L., Dongsheng S. Cheng, Harikrishna Tanjore, Vasiliy V. Polosukhin, Timothy S. Blackwell, and William E. Lawson. "Induction Of Endoplasmic Reticulum Stress Exacerbates Bleomycin Induced Lung Fibrosis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2444.

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Raporty organizacyjne na temat "Endoplasmic reticulum stress"

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Murphy-Ullrich, Joanne E. The Endoplasmic Reticulum Stress Protein Calreticulin in Diabetic Chronic Kidney Disease. Defense Technical Information Center, 2015. http://dx.doi.org/10.21236/ada624022.

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Burke, Robert E. Endoplasmic Reticulum Stress as a Mediator of Neurotoxin-Induced Dopamine Neuron Death. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada430729.

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Burke, Robert E. Endoplasmic Reticulum Stress as a Mediator of Neurotoxin-Induced Dopamine Neuron Death. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada462341.

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Burke, Robert E. Endoplasmic Reticulum Stress as a Mediator of Neurotoxin-Induced Dopamine Neuron Death. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada476094.

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Christopher, David A., and Avihai Danon. Plant Adaptation to Light Stress: Genetic Regulatory Mechanisms. United States Department of Agriculture, 2004. http://dx.doi.org/10.32747/2004.7586534.bard.

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Original Objectives: 1. Purify and biochemically characterize RB60 orthologs in higher plant chloroplasts; 2. Clone the gene(s) encoding plant RB60 orthologs and determine their structure and expression; 3. Manipulate the expression of RB60; 4. Assay the effects of altered RB60 expression on thylakoid biogenesis and photosynthetic function in plants exposed to different light conditions. In addition, we also examined the gene structure and expression of RB60 orthologs in the non-vascular plant, Physcomitrella patens and cloned the poly(A)-binding protein orthologue (43 kDa RB47-like protein).
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