Results 31 to 40 of about 15,125 (218)
Depletion of RIPK3 or MLKL blocks TNF-driven necroptosis and switches towards a delayed RIPK1 kinase-dependent apoptosis [PDF]
, 2014 In human cells, the RIPK1-RIPK3-MLKL-PGAM5-Drp1 axis drives tumor necrosis factor (TNF)-induced necroptosis through mitochondrial fission, but whether this pathway is conserved among mammals is not known. To answer this question, we analyzed the presence Baekelandt, V, Bertrand, Mathieu, Bruggeman, Inge, Dondelinger, Yves, Gonçalves, Amanda, Goossens, Vera, Grootjans, Sasker, Remijsen, Quinten, Roelandt, Ria, Takahashi, Nozomi, Van den Haute, C, Vanden Berghe, Tom, Vandenabeele, Peter, Vanlangenakker, Nele +13 morecore +3 more sourcesMixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis
iScience, 2022 Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C.Yang Liu, Li-Hua Xing, Fen-Xin Li, Na Wang, Yu-Ze Ma, Jian-Wei Li, Yu-Jing Wu, Jing Liang, Yu-Xin Lei, Xue-Yin Wang, Fan-Hua Meng, Yong-Jun Yang, Guang-Peng Li, Xiao Wang, Shui-Xing Yu +14 moredoaj +1 more sourcePUMA amplifies necroptosis signaling by activating cytosolic DNA sensors. [PDF]
, 2018 Necroptosis, a form of regulated necrotic cell death, is governed by RIP1/RIP3-mediated activation of MLKL. However, the signaling process leading to necroptotic death remains to be elucidated.Chen, Dongshi, Stolz, Donna B., Tong, Jingshan, Wei, Liang, Yang, Liheng, Yu, Jian, Zhang, Jianke, Zhang, Lin +7 morecore +2 more sourcesThe brain protection of MLKL inhibitor necrosulfonamide against focal ischemia/reperfusion injury associating with blocking the nucleus and nuclear envelope translocation of MLKL and RIP3K
Frontiers in Pharmacology, 2023 Mixed lineage kinase like protein (MLKL) is a key mediator of necroptosis. While previous studies highlighted the important role of MLKL as one of the central regulators of brain damage against acute ischemic neuronal injury, how the activation of MLKL ...Xian-Yong Zhou, Bo Lin, Wei Chen, Rui-Qi Cao, Yi Guo, Ali Said, Taous Khan, Hui-Ling Zhang, Yong-Ming Zhu +8 moredoaj +1 more sourceEssential versus accessory aspects of cell death: recommendations of the NCCD 2015 [PDF]
, 2014 Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). A Ciechanover, A Criollo, A Degterev, A Degterev, A Degterev, A Gross, A Hochreiter-Hufford, A Kaczmarek, A Linkermann, A Linkermann, A Linkermann, A Linkermann, A Nagasaka, A Oberst, A Oberst, A Pogrebniak, A Rebbaa, A Strasser, A Villunger, AA Fatokun, AA Mailleux, AC Schinzel, AD Dam, AG Fraser, AJ Schile, AM Chinnaiyan, AM Chinnaiyan, AM Choi, AM Verhagen, AU Lindner, AV Vaseva, B D Dynlacht, B Joseph, B La Scola, B La Scola, B Levine, B R Stockwell, B Zhivotovsky, B Zhivotovsky, BA Gibson, BB Wolf, BH Han, C Borner, C Brenner, C Brenner, C Brenner, C Brenner, C Du, C Garrido, C Garrido, C López-Otín, C M Rodrigues, C Munoz-Pinedo, C Muñoz-Pinedo, C Scaffidi, C Scheller, C Volbracht, C Volbracht, CM Haynes, CO Bellamy, CP Baines, CP Baines, CP Dillon, D Adam, D Andrews, D C Rubinsztein, D Chandra, D Denton, D Denton, D Denton, D Denton, D Denton, D E Bredesen, D Grander, D J Klionsky, D R Green, D Raoult, D Ren, D Vercammen, D Vercammen, D Vercammen, D Xue, D Zhu, DA Fruman, DC Rubinsztein, DE Bredesen, DJ Klionsky, DL Berry, DL Vaux, DM Moujalled, DM Moujalled, DM Underhill, DR Green, DR Green, DV Krysko, DV Krysko, DW Zhang, E Basso, E Candi, E F Wagner, E H Baehrecke, E H Cheng, E Laane, E Lugli, E Murphy, E Noch, E S Alnemri, E Tasdemir, E White, E White, EA Minina, EA Slee, EA Slee, EH Baehrecke, EJ Park, F Basit, F Cecconi, F Cecconi, F Gonzalvez, F K Chan, F Madeo, F Pietrocola, F Verrier, FC Kischkel, FH Igney, G A Rabinovich, G Denecker, G Hajnoczky, G Kroemer, G Kroemer, G Kroemer, G Kroemer, G Kroemer, G Kroemer, G Kroemer, G Lettre, G M Fimia, G Marino, G Melino, G Nuñez, G Szabadkai, G Trichonas, G Van Loo, GP Sims, H Gronemeyer, H Ichijo, H Kanuka, H Kenis, H Khalil, H Kim, H L Tang, H Pearson, H Puthalakath, H Puthalakath, H Puthalakath, H Varma, H Wajant, H Walczak, H Walczak, H Wang, H Yoshida, H Zhu, H Zou, H-U Simon, HI Roach, HL Tang, HL Tang, I Amelio, I Martinou, I Vitale, IK Poon, IP Nezis, J A Cidlowski, J E Chipuk, J H Prehn, J Hitomi, J J Lemasters, J Li, J M Abrams, J M Bravo-San Pedro, J M Hardwick, J M Penninger, J Michels, J P Medema, J Sosna, J Wu, J Yang, J Yuan, J Yuan, J Zhao, J-C Marine, J-C Martinou, JA Rickard, JC Reed, JE Chipuk, JE Chipuk, JE Vince, JF Kerr, JG Albeck, JG Albeck, JH Shin, JJ Lemasters, JL Luo, JM Hardwick, JM Murphy, JS Long, JU Schweichel, JW Upton, K Bianchi, K Blomgren, K Kehe, K Kuida, K Kuida, K Miyazaki, K Newton, K Nihira, K Prabhakaran, K Richter, K S Ravichandran, K Segawa, K Tracy, K-M Debatin, KA Spriggs, KC Zimmermann, KN Alavian, KR Knight, L Altucci, L Duprez, L Galluzzi, L Galluzzi, L Galluzzi, L Galluzzi, L Galluzzi, L Galluzzi, L Galluzzi, L Galluzzi, L Galluzzi, L Mondragon, L Steinhart, L Sun, L Zitvogel, LC Gomes, M Ankarcrona, M Annicchiarico-Petruzzelli, M Arundine, M Bonora, M Campanella, M Campanella, M Chautan, M D'Amelio, M E Peter, M Elgendy, M Endres, M Irmler, M J Bertrand, M Leist, M Los, M MacFarlane, M Mediavilla-Varela, M Muzio, M O Hengartner, M Okada, M Overholtzer, M Piacentini, M V Blagosklonny, M Woo, M-L Gougeon, MA Burguillos, MA Hughes, MA Mellen, MA Mellen, MA O'Donnell, MB Jensen, MC Wei, ME Peter, MJ Bertrand, ML Coleman, N Di Daniele, N G Bazan, N Holler, N Honarpour, N Mizushima, N Mizushima, N S Chandel, N Tavernarakis, N Vanlangenakker, N Vanlangenakker, N Vanlangenakker, NJ Curtin, NJ McCarthy, NN Danial, O Kepp, O Kepp, O Krysko, P Bouillet, P Golstein, P J Jost, P Kraft, P Li, P Mazzarello, P Meier, P Nicotera, P Nicotera, P Pacher, P Pinton, P Saikumar, P Schotte, P Vandenabeele, P Vandenabeele, P Vandenabeele, P Vandenabeele, PE Czabotar, PG Clarke, PJ Jost, PS Brookes, Q Remijsen, Q Zhang, R A Flavell, R A Knight, R A Lockshin, R De Maria, R Hakem, R Rashmi, R Rizzuto, R Skouta, R Weinlich, RA Lockshin, RA Lockshin, RC Taylor, RJ O'Brien, RM del Moral, RU Janicke, RW Oppenheim, S A Aaronson, S A Lipton, S Barut, S Bhattacharyya, S Dolma, S Enzenmuller, S Fulda, S Fulda, S Grootjans, S He, S J Martin, S Jouan-Lanhouet, S Kumar, S Kumar, S Melino, S Morioka, S Renolleau, S Tan, S Vallabhapurapu, S W Tait, S Zelenay, SA Lakhani, SA Susin, SB Bratton, SC Chow, SJ Dixon, SJ Dixon, SJ Kim, SJ Martin, SJ Martin, SM Knoblach, SM Laster, SM Srinivasula, SN Willis, SW Tait, SW Tait, SW Tait, SW Tait, SW Tait, SW Yu, SW Yu, SY Chen, T Hirsch, T Ide, T Kaufmann, T Lindsten, T M Dawson, T Nakagawa, T Nakamura, T Panaretakis, T Rudel, T Tenev, T Vanden Berghe, T Vanden Berghe, T Vanden Berghe, T Vanden Berghe, T Vanden Berghe, TG Cotter, TJ Daish, TJ Fan, TM Caserta, U Moll, V De Laurenzi, V Giorgio, V Gogvadze, V L Dawson, V Labi, V M Dixit, V Nikoletopoulou, W Fiers, W G Wood, W Han, W Han, W Hou, W Malorni, W S El-Deiry, W Zhang, WJ Kaiser, WJ Kaiser, WS Yang, WW Chen, X Chen, X Li, X Liu, X Luo, X Pan, XM Yin, Y Ben-Neriah, Y Dondelinger, Y Dondelinger, Y Eguchi, Y Fuchs, Y Li, Y Liu, Y Rong, Y Shi, Y Tsujimoto, Y Wang, Y Zaltsman, YP Ow, YS Cho, Z Cai, Z Song, Z Wang, Z Zakeri, ZA Dunai +438 morecore +21 more sourcesEvolutionary divergence of the necroptosis effector MLKL [PDF]
Cell Death & Differentiation, 2016 The pseudokinase, MLKL (mixed-lineage kinase domain-like), is the most terminal obligatory component of the necroptosis cell death pathway known. Phosphorylation of the MLKL pseudokinase domain by the protein kinase, receptor interacting protein kinase-3 (RIPK3), is known to be the key step in MLKL activation.M C, Tanzer, I, Matti, J M, Hildebrand, S N, Young, A, Wardak, A, Tripaydonis, E J, Petrie, A L, Mildenhall, D L, Vaux, J E, Vince, P E, Czabotar, J, Silke, J M, Murphy +12 moreopenaire +2 more sourcesA RIPK3-independent role of MLKL in suppressing parthanatos promotes immune evasion in hepatocellular carcinoma
Cell Discovery, 2023 Mixed lineage kinase domain-like (MLKL) is widely accepted as an executioner of necroptosis, in which MLKL mediates necroptotic signaling and triggers cell death in a receptor-interacting protein kinase 3 (RIPK3)-dependent manner.Xifei Jiang, Wenjia Deng, Siyao Tao, Zheng Tang, Yuehong Chen, Mengxin Tian, Ting Wang, Chenyang Tao, Yize Li, Yuan Fang, Congying Pu, Jun Gao, Xiaomin Wang, Weifeng Qu, Xiameng Gai, Zhenbin Ding, Yixian Fu, Ying Zheng, Siyuwei Cao, Jian Zhou, Min Huang, Weiren Liu, Jun Xu, Jia Fan, Yinghong Shi +24 moredoaj +1 more sourceThe necroptosis-inducing pseudokinase mixed lineage kinase domain-like regulates the adipogenic differentiation of pre-adipocytes
iScience, 2022 Summary: Receptor-interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like (MLKL) proteins are key regulators of necroptosis, a highly pro-inflammatory mode of cell death, which has been involved in various human diseases.Julie Magusto, Carine Beaupère, Marta B. Afonso, Martine Auclair, Jean-Louis Delaunay, Pierre-Antoine Soret, Gilles Courtois, Tounsia Aït-Slimane, Chantal Housset, Isabelle Jéru, Bruno Fève, Vlad Ratziu, Cecilia M.P. Rodrigues, Jérémie Gautheron +13 moredoaj +1 more source
