Littérature scientifique sur le sujet « RIPK3-MLKL-necroptotic pathway »
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Articles de revues sur le sujet "RIPK3-MLKL-necroptotic pathway"
Ji, Y., L. A. Ward et C. J. Hawkins. « Reconstitution of Human Necrosome Interactions in Saccharomyces cerevisiae ». Biomolecules 11, no 2 (25 janvier 2021) : 153. http://dx.doi.org/10.3390/biom11020153.
Texte intégralYang, Fang-Hao, Xiao-Lei Dong, Guo-Xiang Liu, Lei Teng, Lin Wang, Feng Zhu, Feng-Hua Xu et al. « The protective effect of C-phycocyanin in male mouse reproductive system ». Food & ; Function 13, no 5 (2022) : 2631–46. http://dx.doi.org/10.1039/d1fo03741b.
Texte intégralPetrie, Emma J., Richard W. Birkinshaw, Akiko Koide, Eric Denbaum, Joanne M. Hildebrand, Sarah E. Garnish, Katherine A. Davies et al. « Identification of MLKL membrane translocation as a checkpoint in necroptotic cell death using Monobodies ». Proceedings of the National Academy of Sciences 117, no 15 (31 mars 2020) : 8468–75. http://dx.doi.org/10.1073/pnas.1919960117.
Texte intégralMurphy, James M., et James E. Vince. « Post-translational control of RIPK3 and MLKL mediated necroptotic cell death ». F1000Research 4 (19 novembre 2015) : 1297. http://dx.doi.org/10.12688/f1000research.7046.1.
Texte intégralTian, Qing, Bo Qin, Yufan Gu, Lijun Zhou, Songfeng Chen, Song Zhang, Shuhao Zhang, Qicai Han, Yong Liu et Xuejian Wu. « ROS-Mediated Necroptosis Is Involved in Iron Overload-Induced Osteoblastic Cell Death ». Oxidative Medicine and Cellular Longevity 2020 (16 octobre 2020) : 1–22. http://dx.doi.org/10.1155/2020/1295382.
Texte intégralSamson, André L., Sarah E. Garnish, Joanne M. Hildebrand et James M. Murphy. « Location, location, location : A compartmentalized view of TNF-induced necroptotic signaling ». Science Signaling 14, no 668 (2 février 2021) : eabc6178. http://dx.doi.org/10.1126/scisignal.abc6178.
Texte intégralSpeir, Mary, Joanne A. O'Donnell, Alyce A. Chen, Akshay A. D'Cruz et Ben A. Croker. « Ptpn6 Inhibits IL-1 Release from Neutrophils By Regulation of Caspase-8- and Ripk3/Mlkl-Dependent Forms of Cell Death ». Blood 132, Supplement 1 (29 novembre 2018) : 274. http://dx.doi.org/10.1182/blood-2018-99-120197.
Texte intégralHuang, Ming, Shuai Zhu, Huihui Huang, Jinzhao He, Kenji Tsuji, William W. Jin, Dongping Xie et al. « Integrin-Linked Kinase Deficiency in Collecting Duct Principal Cell Promotes Necroptosis of Principal Cell and Contributes to Kidney Inflammation and Fibrosis ». Journal of the American Society of Nephrology 30, no 11 (25 octobre 2019) : 2073–90. http://dx.doi.org/10.1681/asn.2018111162.
Texte intégralPicon, Carmen, Anusha Jayaraman, Rachel James, Catriona Beck, Patricia Gallego, Maarten E. Witte, Jack van Horssen, Nicholas D. Mazarakis et Richard Reynolds. « Neuron-specific activation of necroptosis signaling in multiple sclerosis cortical grey matter ». Acta Neuropathologica 141, no 4 (10 février 2021) : 585–604. http://dx.doi.org/10.1007/s00401-021-02274-7.
Texte intégralChen, Jing, Renate Kos, Johan Garssen et Frank Redegeld. « Molecular Insights into the Mechanism of Necroptosis : The Necrosome as a Potential Therapeutic Target ». Cells 8, no 12 (21 novembre 2019) : 1486. http://dx.doi.org/10.3390/cells8121486.
Texte intégralThèses sur le sujet "RIPK3-MLKL-necroptotic pathway"
Alì, Alessandra. « Studies on molecular aspects of inflammation : Involvement of purinergic P2X7R in collagen production in systemic sclerosis and chronic heart failure Neutrophil Extracellular Traps release in synovial fluid from microcrystal and non-microcrystal arthritis ». Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071012.
Texte intégralBackground: A novel neutrophils defense mechanism discovered in recent years consists in the extracellular release of network consisting of DNA associated with histones and neutrophils granule enzymes in the form of Neutrophil Extracellular Traps (NETs). Although NETs were originally recognized as a host defence mechanism in which neutrophils release their nuclear and granular contents to kill pathogens, today it is know that NETs are also involved in the pathogenesis of autoimmune and inflammatory diseases, including microcrystalline arthropathies such as gout and pseudogout. Objective and Methods: The aim of this study is to characterize NETs formation in synovial fluid of patients affected by microcrystal arthritis (gout and pseudogout caused, respectively, by MSU or CPPD crystals) compared to that of arthritis not induced by microcrystals (rheumatoid arthritis, psoriatic arthritis). Our first step was to separate neutrophils from other cells present in synovial fluid of gout, pseudogout and non-microcrystal arthritis samples obtained through arthrocentesis. In order to pursue our goal in these samples we evaluated: -the presence of NETs using an immunofluorescence technique; -the amount of NETs released through a fluorimetric assay measuring extracellular DNA; -the levels of pro-inflammatory cytokines and Neutrophil Elastase (NE) by ELISA test. The potential involvement of RIPK3-MLKL-activated necroptotic pathway in NETs formation were also investigated through the analysis of phosphorylated (p)-MLKL, measured by Western Blot technique. In vitro experiments were also performed to evaluate how neutrophils separated from peripheral blood of healthy donors undergo NETs formation when incubated with MSU or CPPD crystals. Results: The experiments performed in this study showed: -microscope images of NETs structures released by neutrophils obtained from synovial fluid of both microcrystal-induced arthritis and non-microcrystal arthritis; -fluorimetric measurement of NETs released directly correlated to microcrystals concentration present in the synovial fluid; -elevated level of IL-6 in both microcrystal and non-microcrystal arthritis; higher IL-1β, IL-8 and IL-10 concentrations in samples from microcrystal-induced arthritis containing a huge amounts of NETs, respect to microcrystal arthritis samples containing low amounts of NETs and non-microcrystal arthritis; -phosphorylation of MLKL, as an index of necroptotic pathway activation in both microcrystal e non-microcrystal arthritis. In vitro experiments confirmed ex vivo data: -increasing concentrations of MSU and CPPD crystals induce NETs release and necroptosis activation in a dose-dependent manner. Conclusions: In conclusions our data provide evidence of NETs formation in synovial fluid of patients affected by gout, pseudogout and non-microcrystal arthritis. Interestingly, NETs formation appears higher in microcrystal arthritis samples and directly correlates with microcrystals (MSU or CPPD) present in synovial fluid of gout and pseudogout patients. Moreover, activation of RIPK3-MLKL necroptotic pathway seems to be involved in NETs production in all these diseases. Therefore, our study pointed out the importance of RIPK3-MLKL activation in NETs release suggesting this pathway as a potential target to regulate NETs cascade in microcrystal and non-microcrystal arthritis.