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3 results on '"Tait, Stephen W.G."'

1. Mitochondrial <scp>DNA</scp> in inflammation and immunity

Author

Riley, Joel S. and Tait, Stephen W.G.

Subjects
Mitochondrial DNA, Immunology, Review, Biology, Mitochondrion, DNA, Mitochondrial, Biochemistry, Genome, 03 medical and health sciences, 0302 clinical medicine, Immunity, Genetics, medicine, Humans, Molecular Biology, 030304 developmental biology, Inflammation, 0303 health sciences, Innate immune system, mtDNA, Pattern recognition receptor, TLR9, Inflammasome, immunity, Immunity, Innate, Mitochondria, Cell biology, cell death, Receptors, Pattern Recognition, Autophagy & Cell Death, 030217 neurology & neurosurgery, medicine.drug
Abstract

Mitochondria are cellular organelles that orchestrate a vast range of biological processes, from energy production and metabolism to cell death and inflammation. Despite this seemingly symbiotic relationship, mitochondria harbour within them a potent agonist of innate immunity: their own genome. Release of mitochondrial DNA into the cytoplasm and out into the extracellular milieu activates a plethora of different pattern recognition receptors and innate immune responses, including cGAS‐STING, TLR9 and inflammasome formation leading to, among others, robust type I interferon responses. In this Review, we discuss how mtDNA can be released from the mitochondria, the various inflammatory pathways triggered by mtDNA release and its myriad biological consequences for health and disease., Mitochondrial DNA is increasingly recognized as a potent agonist of innate immunity. This review discusses how mitochondrial DNA can be released from mitochondria and trigger the activation of different pro‐inflammatory signaling pathways.

Published
2020

2. 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 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, 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, Manic, Gwenola, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, Edward A., Molkentin, Jeffery D., Moll, Ute M., Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, 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, Vander Heiden, Matthew G., Villunger, Andreas, Virgin, Herbert W., 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, Melino, Gerry, and Kroemer, Guido

Subjects
ddc
Published
2018

3. Parkin-Independent Mitophagy Controls Chemotherapeutic Response in Cancer Cells

Author

Villa, Elodie, Proïcs, Emma, Rubio-Patiño, Camila, Obba, Sandrine, Zunino, Barbara, Bossowski, Jozef P., Rozier, Romain M., Chiche, Johanna, Mondragón, Laura, Riley, Joel S., Marchetti, Sandrine, Verhoeyen, Els, Tait, Stephen W.G., and Ricci, Jean-Ehrland

Subjects
Cell Death, Protein Stability, PINK1, Ubiquitin-Protein Ligases, Mitophagy, chemoresistance, mtKeima, Antineoplastic Agents, Mitochondria, ARIH1, Parkin-independent, lung cancer, lcsh:Biology (General), Cytoprotection, Cell Line, Tumor, Neoplasms, Autophagy, Humans, Carrier Proteins, lcsh:QH301-705.5, Protein Kinases, E3 ligase, RBR-ligase, HeLa Cells
Abstract

Mitophagy is an evolutionarily conserved process that selectively targets impaired mitochondria for degradation. Defects in mitophagy are often associated with diverse pathologies, including cancer. Because the main known regulators of mitophagy are frequently inactivated in cancer cells, the mechanisms that regulate mitophagy in cancer cells are not fully understood. Here, we identified an E3 ubiquitin ligase (ARIH1/HHARI) that triggers mitophagy in cancer cells in a PINK1-dependent manner. We found that ARIH1/HHARI polyubiquitinates damaged mitochondria, leading to their removal via autophagy. Importantly, ARIH1 is widely expressed in cancer cells, notably in breast and lung adenocarcinomas; ARIH1 expression protects against chemotherapy-induced death. These data challenge the view that the main regulators of mitophagy are tumor suppressors, arguing instead that ARIH1-mediated mitophagy promotes therapeutic resistance.

Published
2017

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