Results 111 to 120 of about 19,353 (245)
Macrophage RIPK3 triggers inflammation and cell death via the XBP1–Foxo1 axis in liver ischaemia–reperfusion injury
JHEP Reports, 2023 Background & Aims Receptor-interacting serine/threonine-protein kinase 3 (RIPK3) is a central player in triggering necroptotic cell death. However, whether macrophage RIPK3 may regulate NOD1-dependent inflammation and calcineurin/transient receptor ...Xiaoye Qu, T. Yang, Xiao Wang, Dongwei Xu, Ye Yu, Jun Li, Long-feng Jiang, Q. Xia, D. Farmer, B. Ke +9 moresemanticscholar +1 more sourceRole of RIPK1/RIPK3/MLKL signalling pathway in sepsis‐associated acute kidney injury
Experimental Physiology, EarlyView.Abstract
Sepsis‐associated acute kidney injury (SA‐AKI) is a common clinical syndrome in critically ill patients, and its high mortality rate is closely related to complex pathological mechanisms. Existing studies have shown that the pathophysiological process of SA‐AKI involves complex multi‐mechanism interactions, including an uncontrolled systemic ...Huijun Yin, Jingyi Wang, Huirong Hanwiley +1 more sourceSalt-inducible kinases inhibitor HG-9-91-01 targets RIPK3 kinase activity to alleviate necroptosis-mediated inflammatory injury
Cell Death and Disease, 2022 Receptor-interacting protein kinase 3 (RIPK3) functions as a central regulator of necroptosis, mediating signaling transduction to activate pseudokinase mixed lineage kinase domain-like protein (MLKL) phosphorylation. Increasing evidences show that RIPK3 Dongxuan Huang, Pengfei Chen, Guoqing Huang, Huimin Sun, Xiaohua Luo, Chaowen He, Fei Chen, Yong Wang, Changchun Zeng, Lianhui Su, Xiaobin Zeng, Jiachun Lu, Shiyue Li, Dongsheng Huang, Hanchao Gao, Mengtao Cao +15 moredoaj +1 more sourceMolecular mechanisms of cell death:recommendations of the Nomenclature Committee on Cell Death 2018 [PDF]
, 2018 Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.Aaronson, Stuart A., Abrams, John M., Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V., Arama, Eli, Baehrecke, Eric H., Barlev, Nickolai A., Bazan, Nicolas G., Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Katiuscia, Blagosklonny, Mikhail V., Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K. -M., Chandel, Navdeep S., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Cohen, Gerald M., Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D'Angiolella, Vincenzo, Dawson, Ted M., Dawson, Valina L., De laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M., Dixon, Scott J., Duckett, Colin S., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Fimia, Gian Maria, Fulda, Simone, Galluzzi, Lorenzo, Garcia-Saez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. Marie, Harris, Isaac S., Heiden, Matthew G. Vander, Hengartner, Michael O., Hetz, Claudio, Ichijo, Hidenori, Jaattela, Marja, Joseph, Bertrand, Jost, Philipp J., Juin, Philippe P., Kaiser, William J., Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Knight, Richard A., Kroemer, Guido, Kumar, Sharad, Lee, Sam W., Lemasters, John J., Levine, Beth, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., Lopez-Otin, Carlos, Lowe, Scott W., Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Molkentin, Jeffery D., Moll, Ute M., Munoz-Pinedo, Cristina, Nagata, Shigekazu, Nunez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Piacentini, Mauro, Pinton, Paolo, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rehm, Markus, Rizzuto, Rosario, Rodrigues, Cecilia M. P., Rubinsztein, David C., Rudel, Thomas, Ryan, Kevin M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, Brent R., Strasser, Andreas, Szabadkai, Gyorgy, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Boris, Vanden Berghe, Tom, Vandenabeele, Peter, Villunger, Andreas, Virgin, Herbert W., Vitale, Ilio, Vousden, Karen H., Vucic, Domagoj, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, James A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Boris, Zitvogel, Laurence +168 morecore +25 more sourcesThe mitochondrial‐targeted antioxidant SkQ1 prevents skeletal muscle mitochondrial‐apoptotic but not necroptotic signalling during ovarian cancer
The Journal of Physiology, EarlyView.Abstract figure legend An evaluation of the degree to which mitochondrial hydrogen peroxide emission (mH2O2)‐mediated apoptotic and necroptotic signalling contributes to skeletal muscle atrophy in an orthotopic epithelial ovarian cancer (EOC) model. To determine whether attenuating mH2O2 could prevent regulated cell death signalling and mitigate muscle Shahrzad Khajehzadehshoushtar, Luca J. Delfinis, Fasih A. Rahman, Madison C. Garibotti, Shivam Gandhi, Aditya N. Brahmbhatt, Brooke A. Morris, Bianca Garlisi, Sylvia Lauks, Caroline Aitken, Leslie Ogilvie, Zhu‐Xu Zhang, Jeremy A. Simpson, Joe Quadrilatero, Jim Petrik, Christopher G. R. Perry +15 morewiley +1 more sourceSibiriline, a new small chemical inhibitor of receptor-interacting protein kinase 1, prevents immune-dependent hepatitis [PDF]
, 2017 Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor-interacting protein kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway.Afonso, Bali, Berger, Biton, Christofferson, Conrad, Dara, Degterev, Degterev, Degterev, Dondelinger, Dondelinger, Duprez, Fabian, Fauster, Filliol, Gautheron, Günther, Harris, Harris, Harris, Hildebrand, Jouan-Lanhouet, Kopalli, Li, Li, Malhi, Miao, Murphy, Najjar, Oberst, Ramachandran, Ren, Roychowdhury, Saeed, Selig, Sun, Takahashi, Takemoto, Teng, Tiegs, Vanden Berghe, Vercammen, Wang, Wang, Xie, Zhao, Zhou +47 morecore +5 more sourcesRIPK3 activation promotes DAXX‐dependent neuronal necroptosis after intracerebral hemorrhage in mice
CNS Neuroscience & Therapeutics, 2023 Necroptosis induced by receptor‐interacting protein kinase 3 (RIPK3) is engaged in intracerebral hemorrhage (ICH) pathology. In this study, we explored the impact of RIPK3 activation on neuronal necroptosis and the mechanism of the death domain ...Qingqing Bai, Shuoyang Wang, D. Rao, Zhiming Zhou, Jianfei Wang, Qi Wang, Yu Qin, Zhaohu Chu, Shoucai Zhao, Dijing Yu, Yang Xu +10 moresemanticscholar +1 more sourceRIPK3 Facilitates Host Resistance to Oral Toxoplasma gondii Infection
Infection and Immunity, 2021 Toxoplasma gondiiinfection activates pattern recognition receptor (PRR) pathways that drive innate inflammatory responses to control infection. Necroptosis is a proinflammatory cell death pathway apart from the innate immune response that has evolved to control pathogenic infection.Patrick W. Cervantes, Bruno Martorelli Di Genova, Billy Joel Erazo Flores, Laura J. Knoll +3 moreopenaire +3 more sourcesKinase-independent function of RIP1, critical for mature T-cell survival and proliferation. [PDF]
, 2016 The death receptor, Fas, triggers apoptotic death and is essential for maintaining homeostasis in the peripheral lymphoid organs. RIP1 was originally cloned when searching for Fas-binding proteins and was later shown to associate also with the signaling ...Bertin, John, Cai, Yubo, Dowling, John P., Gough, Peter J., Zhang, Jianke +4 morecore +2 more sources
