Добірка наукової літератури з теми "Sephin1, autophagy, integrated stress response"
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Статті в журналах з теми "Sephin1, autophagy, integrated stress response"
Ruiz, Asier, Jone Zuazo, Carolina Ortiz-Sanz, Celia Luchena, Carlos Matute, and Elena Alberdi. "Sephin1 Protects Neurons against Excitotoxicity Independently of the Integrated Stress Response." International Journal of Molecular Sciences 21, no. 17 (August 24, 2020): 6088. http://dx.doi.org/10.3390/ijms21176088.
Повний текст джерелаKroemer, Guido, Guillermo Mariño, and Beth Levine. "Autophagy and the Integrated Stress Response." Molecular Cell 40, no. 2 (October 2010): 280–93. http://dx.doi.org/10.1016/j.molcel.2010.09.023.
Повний текст джерелаChen, Yanan, Joseph R. Podojil, Rejani B. Kunjamma, Joshua Jones, Molly Weiner, Wensheng Lin, Stephen D. Miller, and Brian Popko. "Sephin1, which prolongs the integrated stress response, is a promising therapeutic for multiple sclerosis." Brain 142, no. 2 (January 17, 2019): 344–61. http://dx.doi.org/10.1093/brain/awy322.
Повний текст джерелаPecoraro, Annalisa, Martina Pagano, Giulia Russo, and Annapina Russo. "Role of Autophagy in Cancer Cell Response to Nucleolar and Endoplasmic Reticulum Stress." International Journal of Molecular Sciences 21, no. 19 (October 4, 2020): 7334. http://dx.doi.org/10.3390/ijms21197334.
Повний текст джерелаSønstevold, Tonje, Nikolai Engedal, Ýrr Mørch, Tore Geir Iversen, Tore Skotland, Kirsten Sandvig, and Maria L. Torgersen. "Structural Variants of poly(alkylcyanoacrylate) Nanoparticles Differentially Affect LC3 and Autophagic Cargo Degradation." Journal of Biomedical Nanotechnology 16, no. 4 (April 1, 2020): 432–45. http://dx.doi.org/10.1166/jbn.2020.2906.
Повний текст джерелаGambardella, Gennaro, Leopoldo Staiano, Maria Nicoletta Moretti, Rossella De Cegli, Luca Fagnocchi, Giuseppe Di Tullio, Sara Polletti, et al. "GADD34 is a modulator of autophagy during starvation." Science Advances 6, no. 39 (September 2020): eabb0205. http://dx.doi.org/10.1126/sciadv.abb0205.
Повний текст джерелаKhandros, Eugene, Christopher S. Thom, Janine D'Souza та Mitchell J. Weiss. "Integrated protein quality-control pathways regulate free α-globin in murine β-thalassemia". Blood 119, № 22 (31 травня 2012): 5265–75. http://dx.doi.org/10.1182/blood-2011-12-397729.
Повний текст джерелаPike, Luke R. G., Dean C. Singleton, Francesca Buffa, Olga Abramczyk, Kanchan Phadwal, Ji-Liang Li, Anna Katharina Simon, James T. Murray, and Adrian L. Harris. "Transcriptional up-regulation of ULK1 by ATF4 contributes to cancer cell survival." Biochemical Journal 449, no. 2 (December 14, 2012): 389–400. http://dx.doi.org/10.1042/bj20120972.
Повний текст джерелаClarke, Robert, Katherine L. Cook, Rong Hu, Caroline O. B. Facey, Iman Tavassoly, Jessica L. Schwartz, William T. Baumann, et al. "Endoplasmic Reticulum Stress, the Unfolded Protein Response, Autophagy, and the Integrated Regulation of Breast Cancer Cell Fate." Cancer Research 72, no. 6 (March 14, 2012): 1321–31. http://dx.doi.org/10.1158/0008-5472.can-11-3213.
Повний текст джерелаMuftuoglu, Muharrem, Po Yee Mak, Vivian Ruvolo, Yuki Nishida, Peter P. Ruvolo, Bing Z. Carter, and Michael Andreeff. "High Dimensional Interrogation of Stress Response Patterns and Cell Death Modes in AML." Blood 136, Supplement 1 (November 5, 2020): 15. http://dx.doi.org/10.1182/blood-2020-143371.
Повний текст джерелаДисертації з теми "Sephin1, autophagy, integrated stress response"
Frapporti, Giulia. "Lysosome orchestrates autophagy and integrated stress response: new insights from Sephin1." Doctoral thesis, Università degli studi di Trento, 2023. https://hdl.handle.net/11572/363904.
Повний текст джерелаSujobert, Pierre. "Ciblage thérapeutique d'AMPK dans les leucémies aiguës myéloïdes." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05S017/document.
Повний текст джерелаAcute myeloid leukemia (AML) is a heterogeneous disease with poor prognosis despite intensive treatments. Virtually all recurrent molecular alterations in AML functionally converge to cause signal transduction pathway dysregulation that drives cellular proliferation and survival. The mammalian target of rapamycin complex 1 (mTORC1) is a rapamycin-sensitive signaling node defined by the interaction between mTOR and raptor. Constitutive mTORC1 activity is nearly universal in AML. However, pharmacologic inhibition with rapamycin or second-generation mTOR kinase inhibitors has shown limited anti-leukemic activity in both preclinical models as well as in clinical trials, suggesting that addiction to this oncogene is not a recurrent event in AML. Here we report that sustained mTORC1 activity is nonetheless essential for the cytotoxicity induced by pharmacologic activation of AMP-activated protein kinase (AMPK) in AML. Our studies employed a novel AMPK activator called GSK621. Using CRISPR/Cas9 and shRNA-mediated silencing of the AMPKa1 catalytic subunit, we showed that AMPK activity was necessary for the anti-leukemic response induced by this agent. GSK621-induced AMPK activation precipitated autophagy, and blocking autophagy via shRNA-mediated knockdown of ATG5 or ATG7 protected AML cells from cytotoxicity resulting from treatment with GSK621, suggesting that autophagy promotes cell death in the context of active AMPK. GSK621 cytotoxicity was consistently observed across twenty different AML cell lines, primary AML patient samples and AML xenografts in vivo. GSK621-induced AMPK activation also impaired the self-renewal capacity of MLL-ENL- and FLT3-ITD-induced murine leukemias as measured by serial methylcellulose replating assays. Strikingly, GSK621 did not induce cytotoxicity in normal CD34+ hematopoietic progenitor cells. We hypothesized that the differential sensitivity to GSK621 could be due to the difference in amplitude of mTORC1 activation between AML and normal CD34+ cells. In contrast to most reported cellular models in which AMPK inhibits mTORC1, sustained mTORC1 activity was seen following GSK621-induced AMPK activation in AML. Inhibition of mTORC1 either pharmacologically (using rapamycin) or genetically (using shRNAs targeting raptor and mTOR) abrogated AMPK-induced cytotoxicity in AML cells, including primary AML patient samples. The same synthetic lethality could be recapitulated in normal CD34+ progenitors by constitutive activation of mTORC1 using a lentivirally-transduced myrAKT construct. We further observed that the level of ATF4 protein is under a transcriptionnal control by mTORC1 and a translational control by AMPK (through eIF2A), and explains the synthetic lethal relationship between AMPK and mTORC1. Taken together, these data show that the magnitude of mTORC1 activity determines the degree of cytotoxicity triggered by AMPK activation. Our results therefore support AMPK activation as a promising therapeutic strategy in AML and other mTORC1-active malignancies which warrants further investigations in clinical trials
"Role of integrated stress response in the progression of liver disease." Tulane University, 2021.
Знайти повний текст джерелаAlcoholic and nonalcoholic fatty liver disease is projected to be the most common cause of liver disease in developing countries. The main significant risk factors are obesity, diabetes mellitus type 2, cardiovascular disease, and dyslipidemia. Louisiana is ranked seventh in liver cancer diagnoses and ranked sixth in the leading cause of death. Recent findings indicated that multifaceted stress response due to the accumulation of fatty acids from the diet is the driving force of disease progression. We sought to study multifaceted integrated stress response (ISR) in liver cells cultured with saturated fatty acids. Understanding the process that ISR takes to either induce or inhibit autophagy, self-eating machinery, in strongly permissive HUH 7.5 cells is vital when treating liver abnormalities. The major protein kinase, P-EIF2 alpha, was the targeted factor contributing the most to autophagy due to its functional link to the endoplasmic reticulum, mitochondria, and cellular membrane by further assessment using the inductive drug, Sephin 1. HUH, 7.5 liver cells are treated with increasing amounts of palmitic acid for 24 hours in DMEM with 10% FBS. ISR activated after substantial cellular damage leading to autophagy impairment. The cell culture was assessed for lipid accumulation, and the expression of PKR, IRE1 alpha, PERK, ATF6, P-EIF2 alpha, HRI, MTORC1, GCN2, P62, and LC3B was achieved by immunoblot analysis. Membrane fluidity PKR, lysosomal MTORC1, and protein synthesis GCN2 activated to elicit an integral response to the ISR pathway. Endoplasmic reticulum protein kinases induced in response to UPR activation lead to an integration of the P-EIF2 alpha pathway. Mitochondrial stress heme regulated inhibitor proliferated to provoke an activation in the significant protein kinase leading to autophagy impairment. The P-EIF2 alpha kinase invoked autophagic deficiency even when dephosphorylation was prevented by Sephin 1 drug treatment. ISR constrained autophagy in the liver-derived cell line due to the accumulation of the toxic saturated fatty acid. Keywords: palmitate, autophagy, fatty liver disease, integrated stress response, Sephin 1
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Glory Ogunyinka
Тези доповідей конференцій з теми "Sephin1, autophagy, integrated stress response"
Lehman, Stacey L., Carly M. Sayers, Jiangbin Ye, Lori S. Hart, Deborah O. Ayeni, Albert Koong, and Constantinos Koumenis. "Abstract 2072: The role of the integrated stress response proteins GCN2 and ATF4 in autophagy and tumor migration." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2072.
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