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1,985 results on '"Green, Douglas R."'

2. Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer’s disease and aging

Author

Paudel, Bidur, Jeong, Si-Yeon, Martinez, Carolina Pena, Rickman, Alexis, Haluck-Kangas, Ashley, Bartom, Elizabeth T., Fredriksen, Kristina, Affaneh, Amira, Kessler, John A., Mazzulli, Joseph R., Murmann, Andrea E., Rogalski, Emily, Geula, Changiz, Ferreira, Adriana, Heckmann, Bradlee L., Green, Douglas R., Sadleir, Katherine R., Vassar, Robert, and Peter, Marcus E.

Published
2024
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3. Necroptosis blockade prevents lung injury in severe influenza

Author

Gautam, Avishekh, Boyd, David F., Nikhar, Sameer, Zhang, Ting, Siokas, Ioannis, Van de Velde, Lee-Ann, Gaevert, Jessica, Meliopoulos, Victoria, Thapa, Bikash, Rodriguez, Diego A., Cai, Kathy Q., Yin, Chaoran, Schnepf, Daniel, Beer, Julius, DeAntoneo, Carly, Williams, Riley M., Shubina, Maria, Livingston, Brandi, Zhang, Dingqiang, Andrake, Mark D., Lee, Seungheon, Boda, Raghavender, Duddupudi, Anantha L., Crawford, Jeremy Chase, Vogel, Peter, Loch, Christian, Schwemmle, Martin, Fritz, Lawrence C., Schultz-Cherry, Stacey, Green, Douglas R., Cuny, Gregory D., Thomas, Paul G., Degterev, Alexei, and Balachandran, Siddharth

Published
2024
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4. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Aqeilan, Rami I, Arama, Eli, Baehrecke, Eric H, Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A, Bartek, Jiri, Bazan, Nicolas G, Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Marco E, Blagosklonny, Mikhail V, Blander, J Magarian, Blandino, Giovanni, Blomgren, Klas, Borner, Christoph, Bortner, Carl D, Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, Thomas, Damgaard, Rune Busk, Calin, George A, Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chen, Guo-Qiang, Chen, Quan, Chen, Youhai H, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M, Dawson, Valina L, De Maria, Ruggero, De Strooper, Bart, Debatin, Klaus-Michael, Deberardinis, Ralph J, Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Engeland, Kurt, Fimia, Gian Maria, Galassi, Claudia, Ganini, Carlo, Garcia-Saez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J Marie, Haupt, Ygal, He, Sudan, Heery, David M, Hengartner, Michael O, Hetz, Claudio, Hildeman, David A, Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J, and Kanneganti, Thirumala-Devi

Subjects
Biochemistry and Cell Biology, Biological Sciences, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic health relevance, Good Health and Well Being, Animals, Humans, Apoptosis, Cell Death, Caspases, Carcinogenesis, Mammals, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

8. Mitotic bookmarking by SWI/SNF subunits

Author

Zhu, Zhexin, Chen, Xiaolong, Guo, Ao, Manzano, Trishabelle, Walsh, Patrick J., Wills, Kendall M., Halliburton, Rebecca, Radko-Juettner, Sandi, Carter, Raymond D., Partridge, Janet F., Green, Douglas R., Zhang, Jinghui, and Roberts, Charles W. M.

Published
2023
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11. High RIPK3 expression is associated with a higher risk of early kidney transplant failure

Author

Wahida, Adam, Schmaderer, Christoph, Büttner-Herold, Maike, Branca, Caterina, Donakonda, Sainitin, Haberfellner, Flora, Torrez, Carlos, Schmitz, Jessica, Schulze, Tobias, Seibt, Tobias, Öllinger, Rupert, Engleitner, Thomas, Haller, Bernhard, Steiger, Katja, Günthner, Roman, Lorenz, Georg, Yabal, Monica, Bachmann, Quirin, Braunisch, Matthias C., Moog, Philipp, Matevossian, Edouard, Aßfalg, Volker, Thorban, Stefan, Renders, Lutz, Späth, Martin R., Müller, Roman-Ulrich, Stippel, Dirk L., Weichert, Wilko, Slotta-Huspenina, Julia, von Vietinghoff, Sibylle, Viklicky, Ondrej, Green, Douglas R., Rad, Roland, Amann, Kerstin, Linkermann, Andreas, Bräsen, Jan Hinrich, Heemann, Uwe, and Kemmner, Stephan

Published
2023
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12. Loss of CD4+ T cell-intrinsic arginase 1 accelerates Th1 response kinetics and reduces lung pathology during influenza infection

Author

West, Erin E., Merle, Nicolas S., Kamiński, Marcin M., Palacios, Gustavo, Kumar, Dhaneshwar, Wang, Luopin, Bibby, Jack A., Overdahl, Kirsten, Jarmusch, Alan K., Freeley, Simon, Lee, Duck-Yeon, Thompson, J. Will, Yu, Zu-Xi, Taylor, Naomi, Sitbon, Marc, Green, Douglas R., Bohrer, Andrea, Mayer-Barber, Katrin D., Afzali, Behdad, Kazemian, Majid, Scholl-Buergi, Sabine, Karall, Daniela, Huemer, Martina, and Kemper, Claudia

Published
2023
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14. TRAIL-induced variation of cell signaling states provides nonheritable resistance to apoptosis.

Author

Baskar, Reema, Fienberg, Harris G, Khair, Zumana, Favaro, Patricia, Kimmey, Sam, Green, Douglas R, Nolan, Garry P, Plevritis, Sylvia, and Bendall, Sean C

Abstract

TNFα-related apoptosis-inducing ligand (TRAIL), specifically initiates programmed cell death, but often fails to eradicate all cells, making it an ineffective therapy for cancer. This fractional killing is linked to cellular variation that bulk assays cannot capture. Here, we quantify the diversity in cellular signaling responses to TRAIL, linking it to apoptotic frequency across numerous cell systems with single-cell mass cytometry (CyTOF). Although all cells respond to TRAIL, a variable fraction persists without apoptotic progression. This cell-specific behavior is nonheritable where both the TRAIL-induced signaling responses and frequency of apoptotic resistance remain unaffected by prior exposure. The diversity of signaling states upon exposure is correlated to TRAIL resistance. Concomitantly, constricting the variation in signaling response with kinase inhibitors proportionally decreases TRAIL resistance. Simultaneously, TRAIL-induced de novo translation in resistant cells, when blocked by cycloheximide, abrogated all TRAIL resistance. This work highlights how cell signaling diversity, and subsequent translation response, relates to nonheritable fractional escape from TRAIL-induced apoptosis. This refined view of TRAIL resistance provides new avenues to study death ligands in general.

Published
2019

15. Rapid metabolic regulation of a novel arginine methylation of KCa3.1 attenuates T cell exhaustion.

Author

Sharma, Piyush, primary, Guo, Ao, additional, Boada Romero, Emilio, additional, Poudel, Suresh, additional, Verbist, Katheine C, additional, Palacios, Gustavo, additional, Immadisetty, Kalyan, additional, Chen, Mark J, additional, Haydar, Dalia, additional, Mishra, Ashutosh, additional, Peng, Junmin, additional, Babu, M.Madan, additional, Krenciute, Giedre, additional, Glazer, Evan S, additional, and Green, Douglas R, additional

Published
2024
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16. cBAF complex components and MYC cooperate early in CD8+ T cell fate

Author

Guo, Ao, Huang, Hongling, Zhu, Zhexin, Chen, Mark J., Shi, Hao, Yuan, Sujing, Sharma, Piyush, Connelly, Jon P., Liedmann, Swantje, Dhungana, Yogesh, Li, Zhenrui, Haydar, Dalia, Yang, Mao, Beere, Helen, Yustein, Jason T., DeRenzo, Christopher, Pruett-Miller, Shondra M., Crawford, Jeremy Chase, Krenciute, Giedre, Roberts, Charles W. M., Chi, Hongbo, and Green, Douglas R.

Published
2022
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18. Cell death: Revisiting the roads to ruin.

Author

Green, Douglas R.

Subjects
*CELL death, *CANCER relapse, *TRAFFIC fatalities, *PYROPTOSIS, *APOPTOSIS
Abstract

A paradigm shift in the study of cell death is currently occurring: whereas previously we had always considered that there were "points of no return" in any cell death pathway, we now realize that in many types of active, regulated cell death, this is not the case. We are also learning that cells that "almost die," but nevertheless survive, can transiently take on an altered state, with potential implications for understanding cancer therapies and relapse. In this perspective, we parse the many forms of cell death by analogy to suicide, sabotage, and murder, and consider how cells that might be "instructed" to engage a cell death pathway might nevertheless survive. In this perspective, Douglas Green discusses the many forms of cell death by analogy to suicide, sabotage, and murder and how cells that engage a cell death pathway might still survive. [ABSTRACT FROM AUTHOR]

Published
2024
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19. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, 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 JM, 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, García-Sáez, 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, Hengartner, Michael O, Hetz, Claudio, Ichijo, Hidenori, Jäättelä, 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, Kumar, Sharad, Lee, Sam W, Lemasters, John J, Levine, Beth, Linkermann, Andreas, Lipton, Stuart A, Lockshin, Richard A, López-Otín, Carlos, Lowe, Scott W, Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, and Manic, Gwenola

Subjects
Biochemistry and Cell Biology, Biological Sciences, Animals, Cell Death, Humans, Lysosomes, Mitochondrial Membrane Transport Proteins, Mitochondrial Permeability Transition Pore, Necrosis, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

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. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018

20. Listeria monocytogenes triggers noncanonical autophagy upon phagocytosis, but avoids subsequent growth-restricting xenophagy

Author

Mitchell, Gabriel, Cheng, Mandy I, Chen, Chen, Nguyen, Brittney N, Whiteley, Aaron T, Kianian, Sara, Cox, Jeffery S, Green, Douglas R, McDonald, Kent L, and Portnoy, Daniel A

Subjects
Microbiology, Biological Sciences, Emerging Infectious Diseases, Biodefense, Foodborne Illness, Prevention, Vaccine Related, Infectious Diseases, Digestive Diseases, Infection, Animals, Autophagy, Bacterial Proteins, Cells, Cultured, Cytosol, Host-Pathogen Interactions, Listeria monocytogenes, Macrophages, Membrane Proteins, Mice, Knockout, Mice, Transgenic, Microscopy, Fluorescence, Mutation, Phagocytosis, Phagosomes, Time-Lapse Imaging, Type C Phospholipases, LC3-associated phagocytosis, phospholipases, ActA, bacteria, macrophage
Abstract

Xenophagy is a selective macroautophagic process that protects the host cytosol by entrapping and delivering microbes to a degradative compartment. Both noncanonical autophagic pathways and xenophagy are activated by microbes during infection, but the relative importance and function of these distinct processes are not clear. In this study, we used bacterial and host mutants to dissect the contribution of autophagic processes responsible for bacterial growth restriction of Listeria monocytogenesL. monocytogenes is a facultative intracellular pathogen that escapes from phagosomes, grows in the host cytosol, and avoids autophagy by expressing three determinants of pathogenesis: two secreted phospholipases C (PLCs; PlcA and PlcB) and a surface protein (ActA). We found that shortly after phagocytosis, wild-type (WT) L. monocytogenes escaped from a noncanonical autophagic process that targets damaged vacuoles. During this process, the autophagy marker LC3 localized to single-membrane phagosomes independently of the ULK complex, which is required for initiation of macroautophagy. However, growth restriction of bacteria lacking PlcA, PlcB, and ActA required FIP200 and TBK1, both involved in the engulfment of microbes by xenophagy. Time-lapse video microscopy revealed that deposition of LC3 on L. monocytogenes-containing vacuoles via noncanonical autophagy had no apparent role in restricting bacterial growth and that, upon access to the host cytosol, WT L. monocytogenes utilized PLCs and ActA to avoid subsequent xenophagy. In conclusion, although noncanonical autophagy targets phagosomes, xenophagy was required to restrict the growth of L. monocytogenes, an intracellular pathogen that damages the entry vacuole.

Published
2018

21. Contributors

Author

Aureli, Massimo, primary, Carsana, Emma Veronica, additional, Endo, Yoshinori, additional, Fang, Evandro F., additional, Gilbert, Alexandra, additional, Green, Douglas R., additional, Hadano, Shinji, additional, Hamano, Tadanori, additional, Hattori, Nobutaka, additional, Heckmann, Bradlee L., additional, Ikeda, Yoshio, additional, Iwata, Atsushi, additional, Ji, Changyi, additional, Johnson, Gail V.W., additional, Kataura, Tetsushi, additional, Lin, Heng, additional, Loberto, Nicoletta, additional, Lunghi, Giulia, additional, Makioka, Kouki, additional, Mano, Tatsuo, additional, Miki, Yasuo, additional, Motoi, Yumiko, additional, Mutoh, Tatsuro, additional, Okamoto, Koichi, additional, Ono, Kenjiro, additional, Otomo, Asako, additional, Patrick-Brown, Thale D.J.H., additional, Saiki, Shinji, additional, Sasazawa, Yukiko, additional, Sato, Masayuki, additional, Schmauck-Medina, Tomas, additional, Shimonaka, Shotaro, additional, Sonnino, Sandro, additional, Sugie, Kazuma, additional, Sugimoto, Azusa, additional, Takatama, Masamitsu, additional, Tanji, Kunikazu, additional, Uddin, Mohammad Nasir, additional, Wakabayashi, Koichi, additional, Yamazaki, Tsuneo, additional, and Zhang, Shi-qi, additional

Published
2022
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23. Targeting Histone Demethylases in MYC-Driven Neuroblastomas with Ciclopirox

Author

Yang, Jun, Milasta, Sandra, Hu, Dongli, AlTahan, Alaa M, Interiano, Rodrigo B, Zhou, Junfang, Davidson, Jesse, Low, Jonathan, Lin, Wenwei, Bao, Ju, Goh, Pollyanna, Nathwani, Amit C, Wang, Ruoning, Wang, Yingdi, Ong, Su Sien, Boyd, Vincent A, Young, Brandon, Das, Sourav, Shelat, Anang, Wu, Yinan, Li, Zhenmei, Zheng, Jie J, Mishra, Ashutosh, Cheng, Yong, Qu, Chunxu, Peng, Junmin, Green, Douglas R, White, Stephen, Guy, R Kiplin, Chen, Taosheng, and Davidoff, Andrew M

Subjects
Rare Diseases, Cancer, Neuroblastoma, Pediatric, Genetics, Neurosciences, Pediatric Cancer, Animals, Antifungal Agents, Cell Differentiation, Cell Proliferation, Ciclopirox, Epigenesis, Genetic, Gene Expression Regulation, Enzymologic, Histone Demethylases, Histones, Humans, Mice, Mice, SCID, Oxidative Phosphorylation, Proto-Oncogene Proteins c-myc, Pyridones, RNA, Small Interfering, Transcription, Genetic, Tumor Cells, Cultured, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Histone lysine demethylases facilitate the activity of oncogenic transcription factors, including possibly MYC. Here we show that multiple histone demethylases influence the viability and poor prognosis of neuroblastoma cells, where MYC is often overexpressed. We also identified the approved small-molecule antifungal agent ciclopirox as a novel pan-histone demethylase inhibitor. Ciclopirox targeted several histone demethylases, including KDM4B implicated in MYC function. Accordingly, ciclopirox inhibited Myc signaling in parallel with mitochondrial oxidative phosphorylation, resulting in suppression of neuroblastoma cell viability and inhibition of tumor growth associated with an induction of differentiation. Our findings provide new insights into epigenetic regulation of MYC function and suggest a novel pharmacologic basis to target histone demethylases as an indirect MYC-targeting approach for cancer therapy. Cancer Res; 77(17); 4626-38. ©2017 AACR.

Published
2017

24. Molecular definitions of autophagy and related processes

Author

Galluzzi, Lorenzo, Baehrecke, Eric H, Ballabio, Andrea, Boya, Patricia, Pedro, José Manuel Bravo‐San, Cecconi, Francesco, Choi, Augustine M, Chu, Charleen T, Codogno, Patrice, Colombo, Maria Isabel, Cuervo, Ana Maria, Debnath, Jayanta, Deretic, Vojo, Dikic, Ivan, Eskelinen, Eeva‐Liisa, Fimia, Gian Maria, Fulda, Simone, Gewirtz, David A, Green, Douglas R, Hansen, Malene, Harper, J Wade, Jäättelä, Marja, Johansen, Terje, Juhasz, Gabor, Kimmelman, Alec C, Kraft, Claudine, Ktistakis, Nicholas T, Kumar, Sharad, Levine, Beth, Lopez‐Otin, Carlos, Madeo, Frank, Martens, Sascha, Martinez, Jennifer, Melendez, Alicia, Mizushima, Noboru, Münz, Christian, Murphy, Leon O, Penninger, Josef M, Piacentini, Mauro, Reggiori, Fulvio, Rubinsztein, David C, Ryan, Kevin M, Santambrogio, Laura, Scorrano, Luca, Simon, Anna Katharina, Simon, Hans‐Uwe, Simonsen, Anne, Tavernarakis, Nektarios, Tooze, Sharon A, Yoshimori, Tamotsu, Yuan, Junying, Yue, Zhenyu, Zhong, Qing, and Kroemer, Guido

Subjects
Animals, Autophagy, Caenorhabditis elegans, Drosophila melanogaster, Gene Regulatory Networks, Mice, Saccharomyces cerevisiae, Terminology as Topic, chaperone-mediated autophagy, LC3-associated phagocytosis, microautophagy, mitophagy, xenophagy, LC3‐associated phagocytosis, chaperone‐mediated autophagy, Biological Sciences, Information and Computing Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Over the past two decades, the molecular machinery that underlies autophagic responses has been characterized with ever increasing precision in multiple model organisms. Moreover, it has become clear that autophagy and autophagy-related processes have profound implications for human pathophysiology. However, considerable confusion persists about the use of appropriate terms to indicate specific types of autophagy and some components of the autophagy machinery, which may have detrimental effects on the expansion of the field. Driven by the overt recognition of such a potential obstacle, a panel of leading experts in the field attempts here to define several autophagy-related terms based on specific biochemical features. The ultimate objective of this collaborative exchange is to formulate recommendations that facilitate the dissemination of knowledge within and outside the field of autophagy research.

Published
2017

29. Influenza Virus Z-RNAs Induce ZBP1-Mediated Necroptosis

Author

Zhang, Ting, Yin, Chaoran, Boyd, David F., Quarato, Giovanni, Ingram, Justin P., Shubina, Maria, Ragan, Katherine B., Ishizuka, Takumi, Crawford, Jeremy Chase, Tummers, Bart, Rodriguez, Diego A., Xue, Jia, Peri, Suraj, Kaiser, William J., López, Carolina B., Xu, Yan, Upton, Jason W., Thomas, Paul G., Green, Douglas R., and Balachandran, Siddharth

Published
2020
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30. Oleic acid availability impacts thymocyte preprogramming and subsequent peripheral Treg cell differentiation

Author

Lin, Liangyu, primary, Hu, Mingyuan, additional, Li, Qing, additional, Du, Liming, additional, Lin, Li, additional, Xue, Yueqing, additional, Zheng, Fanjun, additional, Wang, Fei, additional, Liu, Keli, additional, Wang, Yu, additional, Ye, Jiayin, additional, Jiang, Xu, additional, Wang, Xuefeng, additional, Wang, Jiaqi, additional, Zhai, Jingjie, additional, Liu, Benming, additional, Xie, Hongzhen, additional, You, Yanqin, additional, Wang, Jinyong, additional, Kong, Xiangyin, additional, Feng, Dechun, additional, Green, Douglas R., additional, Shi, Yufang, additional, and Wang, Ying, additional

Published
2023
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31. c-Abl Phosphorylates MFN2 to Regulate Mitochondrial Morphology in Cells under Endoplasmic Reticulum and Oxidative Stress, Impacting Cell Survival and Neurodegeneration

Author

Martinez, Alexis, primary, Lamaizon, Cristian M., additional, Valls, Cristian, additional, Llambi, Fabien, additional, Leal, Nancy, additional, Fitzgerald, Patrick, additional, Guy, Cliff, additional, Kamiński, Marcin M., additional, Inestrosa, Nibaldo C., additional, van Zundert, Brigitte, additional, Cancino, Gonzalo I., additional, Dulcey, Andrés E., additional, Zanlungo, Silvana, additional, Marugan, Juan J., additional, Hetz, Claudio, additional, Green, Douglas R., additional, and Alvarez, Alejandra R., additional

Published
2023
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35. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. [0000-0002-4643-0474], Dieter, Adam [0000-0002-5668-5032], Agostini, Massimiliano [0000-0003-3124-2072], Agostinis, Patrizia [0000-0003-1314-2115], Alnemri, Emad S. [0000-0002-7295-3383], Altucci, Lucia [0000-0002-7312-5387], Amelio, Ivano [0000-0002-9126-5391], Andrews, David W. [0000-0002-9266-7157], Aqeilan, Rami I. [0000-0002-6034-023X], Arama, Eli [0000-0001-5953-0629], Balachandran, Siddharth [0000-0003-2084-1803], Bano, Daniele [0000-0002-9617-5504], Bartek, Jiri [0000-0003-2013-7525], Bazan, Nicolas G. [0000-0002-9243-5444], Bernassola, Francesca [0000-0002-8883-8654], Bertrand, Mathieu J. M. [0000-0001-9000-0626], Bianchi, Marco Emilio [0000-0002-5329-6445], Blander, J. Magarian [0000-0001-9207-1700], Blandino, Giovanni [0000-0002-6970-2241], Blomgren, Klas [0000-0002-0476-7271], Bortner, Carl D. [0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. [0000-0002-2915-3970], De Maria, Ruggero [0000-0003-2255-0583], Debatin, Klaus-Michael [0000-0002-8397-1886], Deberardinis, Ralph J. [0000-0002-2705-7432], Degterev, Alexei [0000-0002-8240-7132], Del Sal, Giannino [0000-0003-2185-6003], Deshmukh, Mohanish [0000-0002-2597-5862], Di Virgilio, Francesco [0000-0003-3566-1362], Diederich, Marc [0000-0003-0115-4725], Dixon, Scott J. [0000-0001-6230-8199], El-Deiry, Wafik S. [0000-0002-9577-8266], Elrod, John W. [0000-0003-3925-2224], Engeland, Kurt [0000-0003-3525-0440], Fimia, Gian María [0000-0003-4438-3325], Ganini, Carlo [0000-0002-5839-3965], García-Sáez, Ana J. [0000-0002-3894-5945], Garg, Abhishek D. [0000-0002-9976-9922], Garrido, Carmen [0000-0003-1368-1493], Gavathiotis, Evripidis [0000-0001-6319-8331], Ghosh, Sourav [0000-0001-5990-8708], Green, Douglas R. [0000-0002-7332-1417], Gronemeyer, Hinrich [0000-0001-9454-2449}, Häcker, Georg [0000-0003-1058-5746], Hajnóczky, György [0000-0003-3813-2570], Hardwick, J. 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Magarian, Blandino, Giovanni, Blomgren, Klas, Bomer, Christoph, Bortner, Carl D., Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, T., Damgaard, Rune Busk, Calin, George A., Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K.-M., Chen, Guo‑Qiang, Chen, Quan, Chen, Youhai H., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M., Dawson, Valina L., De Maria, Ruggero, De Strooper, B., Debatin, Klaus-Michael, Deberardinis, Ralph J., Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Engeland, Kurt, Fimia, Gian María, Galassi, Claudia, Ganini, Carlo, García-Sáez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J. Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravinchandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strappazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, G, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

43. CD4 T cell intrinsic arginase 1 controls the kinetics of Th1 induction and contraction

Author

West, Erin E, primary, Merle, Nicolas S, additional, Kamiński, Marcin M, additional, Palacios, Gustavo, additional, Kumar, Dhaneshwar, additional, Wang, Luopin, additional, Overdahl, Kristen, additional, Jarmusch, Alan K, additional, Freeley, Simon, additional, Taylor, Naomi, additional, Sitbon, Marc, additional, Green, Douglas R, additional, Bohrer, Andrea, additional, Mayer-Barber, Katrin, additional, Afzali, Behdad, additional, Kazemian, Majid, additional, Scholl-Buergi, Sabine, additional, Karall, Daniela, additional, Huemer, Martina, additional, and Kemper, Claudia, additional

Published
2023
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48. p53 tumor suppressor gene mutations in fibroblast-like synoviocytes from erosion synovium and non-erosion synovium in rheumatoid arthritis.

Author

Yamanishi, Yuji, Boyle, David L, Green, Douglas R, Keystone, Edward C, Connor, Alison, Zollman, Susan, and Firestein, Gary S

Subjects
Synovial Membrane, Cell Line, Clone Cells, Fibroblasts, Humans, Arthritis, Rheumatoid, Codon, Mutagenesis, Insertional, DNA Mutational Analysis, Sequence Deletion, Mutation, Missense, Point Mutation, Genes, p53, Matrix Metalloproteinase 1, erosion, fibroblast-like synoviocytes, invasiveness, p53 mutation, rheumatoid arthritis, Arthritis, Rheumatoid, Genes, p53, Mutagenesis, Insertional, Mutation, Missense, Clinical Sciences, Immunology, Public Health and Health Services, Arthritis & Rheumatology
Abstract

Abnormalities in the p53 tumor suppressor gene have been detected in rheumatoid arthritis (RA) and could contribute to the pathogenesis of chronic disease. To determine whether synoviocytes from invasive synovium in RA have an increased number of mutations compared with non-erosion synoviocytes, p53 cDNA subclones from fibroblast-like synoviocytes (FLS) derived from erosion and non-erosion sites of the same synovium were examined in patients requiring total joint replacement. Ten erosion FLS lines and nine non-erosion FLS lines were established from nine patients with RA. Exons 5-10 from 209 p53 subclones were sequenced (114 from erosion FLS, 95 from non-erosion FLS). Sixty percent of RA FLS cell lines and 8.6% of the p53 subclones isolated from FLS contained p53 mutations. No significant differences were observed between the erosion and non-erosion FLS with regard to the frequency or type of p53 mutation. The majority of the mutations were missense transition mutations, which are characteristic of oxidative damage. In addition, paired intact RA synovium and cultured FLS from the same joints were evaluated for p53 mutations. Matched synovium and cultured synoviocytes contained p53 mutations, although there was no overlap in the specific mutations identified in the paired samples. Clusters of p53 mutations in subclones were detected in some FLS, including one in codon 249, which is a well-recognized 'hot spot' associated with cancer. Our data are consistent with the hypothesis that p53 mutations are randomly induced by genotoxic exposure in small numbers of RA synoviocytes localized to erosion and non-erosion regions of RA synovium. The determining factor for invasiveness might be proximity to bone or cartilage rather than the presence of a p53 mutation.

Published
2005

50. Disruption of Mitochondrial Function during Apoptosis Is Mediated by Caspase Cleavage of the p75 Subunit of Complex I of the Electron Transport Chain

Author

Ricci, Jean-Ehrland, Muñoz-Pinedo, Cristina, Fitzgerald, Patrick, Bailly-Maitre, Béatrice, Perkins, Guy A, Yadava, Nagendra, Scheffler, Immo E, Ellisman, Mark H, and Green, Douglas R

Subjects
Biochemistry and Cell Biology, Biological Sciences, 1.1 Normal biological development and functioning, Underpinning research, Generic health relevance, Adenosine Triphosphate, Amino Acid Sequence, Animals, Apoptosis, Caspases, Catalytic Domain, Electron Transport Chain Complex Proteins, Electron Transport Complex I, Energy Metabolism, HeLa Cells, Humans, Intracellular Membranes, Mice, Microscopy, Electron, Mitochondria, Molecular Sequence Data, Mutation, NADH Dehydrogenase, Reactive Oxygen Species, Hela Cells, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Mitochondrial outer membrane permeabilization and cytochrome c release promote caspase activation and execution of apoptosis through cleavage of specific caspase substrates in the cell. Among the first targets of activated caspases are the permeabilized mitochondria themselves, leading to disruption of electron transport, loss of mitochondrial transmembrane potential (DeltaPsim), decline in ATP levels, production of reactive oxygen species (ROS), and loss of mitochondrial structural integrity. Here, we identify NDUFS1, the 75 kDa subunit of respiratory complex I, as a critical caspase substrate in the mitochondria. Cells expressing a noncleavable mutant of p75 sustain DeltaPsim and ATP levels during apoptosis, and ROS production in response to apoptotic stimuli is dampened. While cytochrome c release and DNA fragmentation are unaffected by the noncleavable p75 mutant, mitochondrial morphology of dying cells is maintained, and loss of plasma membrane integrity is delayed. Therefore, caspase cleavage of NDUFS1 is required for several mitochondrial changes associated with apoptosis.

Published
2004

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