Results 51 to 60 of about 17,697 (207)

RIPK1 is a critical modulator of both tonic and TLR-responsive inflammatory and cell death pathways in human macrophage differentiation [PDF]

, 2018
In this study, we took advantage of human-induced pluripotent stem cells (hiPSC) and CRISPR/Cas9 technology to investigate the potential roles of RIPK1 in regulating hematopoiesis and macrophage differentiation, proinflammatory activation, and cell death
Buchrieser, Julian, Cowley, Sally A., Long, Joshua C. D., Long, Joshua C. D., Moore, Michael D., Oliva Martín, María José, Pérez Simón, José Antonio, Venero Recio, José Luis   +7 more
core   +1 more source

Tuning Apoptosis and Neuroinflammation: TBK1 Restrains RIPK1 [PDF]

Cell, 2018
Partial loss of TANK-binding kinase 1 (TBK1) causes amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Xu et al. identify the role of TBK1 in suppressing neuroinflammation and apoptosis by its inhibition of the receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and elucidate how aging and genetic susceptibility together ...
Haiyang, Yu, Don W, Cleveland
openaire   +2 more sources

Receptor-interacting protein kinase 1 (RIPK1) regulates cervical cancer cells via NF-κB–TNF-α pathway: An in vitro study

Translational Oncology, 2023
Introduction: Cervical cancer (CC) is associated with high morbidity and mortality rates in women. Members of the receptor-interacting protein kinase (RIPK) family are important regulators of inflammation and cell death.
Wenqi Bai, Fengjie Cui, Zihan Wang, Xianhua Gu, Xiaojing Fang, Li Zhou, Suyang Guo   +6 more
doaj   +1 more source

Necroptosis in bacterial infections

Frontiers in Immunology
Necroptosis, a recently discovered form of cell-programmed death that is distinct from apoptosis, has been confirmed to play a significant role in the pathogenesis of bacterial infections in various animal models. Necroptosis is advantageous to the host,
Xing Yu, Jin Yuan, Linxi Shi, Shuying Dai, Lei Yue, Min Yan   +5 more
doaj   +1 more source

Essential 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 more
core   +17 more sources

Primidone blocks RIPK1-driven cell death and inflammation [PDF]

Cell Death & Differentiation, 2020
AbstractThe receptor-interacting serine/threonine protein kinase 1 (RIPK1) is a key mediator of regulated cell death and inflammation. Recent studies suggest that RIPK1 inhibition would fundamentally improve the therapy of RIPK1-dependent organ damage in stroke, myocardial infarction, kidney failure, and systemic inflammatory response syndrome ...
Riebeling, Theresa, Jamal, Kunzah, Wilson, Rebecca, Kolbrink, Benedikt, von Samson-Himmelstjerna, Friedrich Alexander, Moerke, Caroline, Ramos Garcia, Laura, Dahlke, Eileen, Michels, Friederike, Lühder, Fred, Schunk, Domagoj, Doldi, Philipp, Tyczynski, Bartosz, Kribben, Andreas, Flüh, Charlotte, Theilig, Franziska, Kunzendorf, Ulrich, Meier, Pascal, Krautwald, Stefan   +18 more
openaire   +5 more sources

Sibiriline, 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 more
core   +5 more sources

Preventing necroptosis by scavenging ROS production alleviates heat stress-induced intestinal injury

International Journal of Hyperthermia, 2020
Background Worldwide heat stroke incidence has increased in recent years and is associated with high morbidity and mortality. Therefore, it is critical to identify mechanisms that mediate heat stroke.
Li Li, Hongping Tan, Zhimin Zou, Jian Gong, Junjie Zhou, Na Peng, Lei Su, Marc Maegele, Daozhang Cai, Zhengtao Gu   +9 more
doaj   +1 more source

Kinase-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 more
core   +2 more sources

Cleavage‐Resistant CYLD Protects Against Autoimmune Hepatitis

Advanced Science, EarlyView.
Proteolytic cleavage of the deubiquitinase CYLD emerges as a critical driver of autoimmune hepatitis. TNFα‐induced CYLD loss in macrophages amplifies S100A9‐triggered MAPK activation, leading to excessive chemokine production and hepatic inflammation. Pharmacological inhibition of MEK signaling effectively attenuates experimental disease, highlighting ...
Han Liu, Chen Su, Jianling Liu, Mingyan Xing, Xiaoxia Wu, Lingxia Wang, Xiaoming Zhao, Hanwen Zhang, YangYang Xie, YangYang Wang, Hong Li, Yu Li, Ming Li, Haibing Zhang   +13 more
wiley   +1 more source