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161 results on '"Bertrand, M J"'

1. A New Device for Crossing Chronic Total Occlusions

Author

Riel, L.-P., Dion, S., Charlebois-Ménard, M., Brouillette, M., Bérubé, S., Despatis, M.-A., Benko, A., Clavet, M.-É., Bertrand, M.-J., Geoffroy, P., Tanguay, J.-F., Sasoh, Akihiro, editor, Aoki, Toshiyuki, editor, and Katayama, Masahide, editor

Published
2019
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9. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, Dieter, Agostinis, Patrizia, Alnemri, E. S., Altucci, Lucia, Amelio, Ivano, Andrews, D. W., Annicchiarico-Petruzzelli, Margherita, Antonov, A. V., Arama, Eli, Baehrecke, E. H., Barlev, N. A., Bazan, N. G., Bernassola, Francesca, Bertrand, M. J. M., Bianchi, Katiuscia, Blagosklonny, M. V., Blomgren, Kla, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, F. K. -M., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, Aaron, Cohen, G. M., Conrad, Marcu, Cubillos-Ruiz, J. R., Czabotar, P. E., D’Angiolella, Vincenzo, Dawson, T. M., Dawson, V. L., de Laurenzi, Vincenzo, De Maria Marchiano, Ruggero, Debatin, Klaus-Michael, Deberardinis, R. J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, V. M., Dixon, S. J., Duckett, C. S., Dynlacht, B. D., El-Deiry, W. S., Elrod, J. W., Fimia, Gian Maria, Fulda, Simone, García-Sáez, A. J., Garg, A. D., Garrido, Carmen, Gavathiotis, Evripidi, Golstein, Pierre, Gottlieb, Eyal, Green, D. R., Greene, L. A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. M., Harris, I. S., Hengartner, M. O., Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, P. J., Juin, P. P., Kaiser, W. J., Karin, Michael, Kaufmann, Thoma, Kepp, Oliver, Kimchi, Adi, Kitsis, R. N., Klionsky, D. J., Knight, R. A., Kumar, Sharad, Lee, S. W., Lemasters, J. J., Levine, Beth, Linkermann, Andrea, Lipton, S. A., Lockshin, R. A., López-Otín, Carlo, Lowe, S. W., Luedde, Tom, Lugli, Enrico, Macfarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, S. J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, E. A., Molkentin, J. D., Moll, U. M., Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theochari, Pasparakis, Manoli, Penninger, J. M., Pereira, D. M., Pervaiz, Shazib, Peter, M. E., Piacentini, Mauro, Pinton, Paolo, Prehn, J. H. M., Puthalakath, Hamsa, Rabinovich, G. A., Rehm, Marku, Rizzuto, Rosario, Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, Thoma, Ryan, K. M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, B. R., Strasser, Andrea, Szabadkai, Gyorgy, Tait, S. W. G., Tang, Daolin, Tavernarakis, Nektario, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Bori, Vanden Berghe, Tom, Vandenabeele, Peter, Vander Heiden, M. G., Villunger, Andrea, Virgin, H. W., Vousden, K. H., Vucic, Domagoj, Wagner, E. F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, J. A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Bori, Zitvogel, Laurence, Melino, Gerry, Kroemer, Guido, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Sistigu, Antonella (ORCID:0000-0002-2528-1238), Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, Dieter, Agostinis, Patrizia, Alnemri, E. S., Altucci, Lucia, Amelio, Ivano, Andrews, D. W., Annicchiarico-Petruzzelli, Margherita, Antonov, A. V., Arama, Eli, Baehrecke, E. H., Barlev, N. A., Bazan, N. G., Bernassola, Francesca, Bertrand, M. J. M., Bianchi, Katiuscia, Blagosklonny, M. V., Blomgren, Kla, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, F. K. -M., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, Aaron, Cohen, G. M., Conrad, Marcu, Cubillos-Ruiz, J. R., Czabotar, P. E., D’Angiolella, Vincenzo, Dawson, T. M., Dawson, V. L., de Laurenzi, Vincenzo, De Maria Marchiano, Ruggero, Debatin, Klaus-Michael, Deberardinis, R. J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, V. M., Dixon, S. J., Duckett, C. S., Dynlacht, B. D., El-Deiry, W. S., Elrod, J. W., Fimia, Gian Maria, Fulda, Simone, García-Sáez, A. J., Garg, A. D., Garrido, Carmen, Gavathiotis, Evripidi, Golstein, Pierre, Gottlieb, Eyal, Green, D. R., Greene, L. A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. M., Harris, I. S., Hengartner, M. O., Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, P. J., Juin, P. P., Kaiser, W. J., Karin, Michael, Kaufmann, Thoma, Kepp, Oliver, Kimchi, Adi, Kitsis, R. N., Klionsky, D. J., Knight, R. A., Kumar, Sharad, Lee, S. W., Lemasters, J. J., Levine, Beth, Linkermann, Andrea, Lipton, S. A., Lockshin, R. A., López-Otín, Carlo, Lowe, S. W., Luedde, Tom, Lugli, Enrico, Macfarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, S. J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, E. A., Molkentin, J. D., Moll, U. M., Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theochari, Pasparakis, Manoli, Penninger, J. M., Pereira, D. M., Pervaiz, Shazib, Peter, M. E., Piacentini, Mauro, Pinton, Paolo, Prehn, J. H. M., Puthalakath, Hamsa, Rabinovich, G. A., Rehm, Marku, Rizzuto, Rosario, Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, Thoma, Ryan, K. M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, B. R., Strasser, Andrea, Szabadkai, Gyorgy, Tait, S. W. G., Tang, Daolin, Tavernarakis, Nektario, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Bori, Vanden Berghe, Tom, Vandenabeele, Peter, Vander Heiden, M. G., Villunger, Andrea, Virgin, H. W., Vousden, K. H., Vucic, Domagoj, Wagner, E. F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, J. A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Bori, Zitvogel, Laurence, Melino, Gerry, Kroemer, Guido, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), and Sistigu, Antonella (ORCID:0000-0002-2528-1238)

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

12. PAYSAGE ET ANALYSE SÉMIOLOGIQUE: DISCUSSION

Author

Berdoulay, V., Bertrand, M.-J., Brunet, R., Claval, P., Dollfus, O., Durand-Dastès, F., Fel, A., Metton, A., Piveteau, J. L., Raffestin, C., Robic, Rougerie, G., and Vanduick, Mlle R.

Published
1974

16. P685In vivo near-infrared fluorescence (NIRF) molecular imaging of atherosclerosis

Author

Bertrand, M.-J., primary, Abran, M., additional, Maafi, F., additional, Busseuil, D., additional, Merlet, N., additional, Mihalache-Avram, T., additional, Tardif, P.-L., additional, Geoffroy, P., additional, Ni, F., additional, Abulrob, A., additional, Lavoie-L'allier, P., additional, Rheaume, E., additional, Lesage, F., additional, and Tardif, J.-C., additional

Published
2017
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19. Essential versus accessory aspects of cell death: Recommendations of the NCCD 2015

Author

Galluzzi, L., Bravo-San Pedro, J. M., Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, D., Alnemri, E. S., Altucci, L., Andrews, D., Annicchiarico-Petruzzelli, M., Baehrecke, E. H., Bazan, N. G., Bertrand, M. J., Bianchi, K., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Campanella, M., Candi, E., Cecconi, F., Chan, F. K., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, A., Dawson, T. M., Dawson, V. L., De Laurenzi, V., De Maria Marchiano, Ruggero, Debatin, K. -M., Di Daniele, N., Dixit, V. M., Dynlacht, B. D., El-Deiry, W. S., Fimia, G. M., Flavell, R. A., Fulda, S., Garrido, C., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnoczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Joseph, B., Jost, P. J., Kaufmann, T., Kepp, O., Klionsky, D. J., Knight, R. A., Kumar, S., Lemasters, J. J., Levine, B., Linkermann, A., Lipton, S. A., Lockshin, R. A., López-Otín, C., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C., Martin, S. J., Martinou, J. -C., Medema, Jan Paul, Meier, P., Melino, S., Mizushima, N., Moll, U., Muñoz-Pinedo, C., Nuñez, G., Oberst, A., Panaretakis, T., Penninger, J. M., Peter, M. E., Piacentini, M., Calzavara Pinton, Piergiacomo, Prehn, J. H., Puthalakath, H., Rabinovich, G. A., Ravichandran, K. S., Rizzuto, R., Rodrigues, C. M., Rubinsztein, D. C., Rudel, T., Shi, Y., Simon, H. -U., Stockwell, B. R., Szabadkai, G., Tait, S. W., Tang, H. L., Tavernarakis, N., Tsujimoto, Y., Vanden Berghe, T., Vandenabeele, P., Villunger, A., Wagner, E. F., Walczak, H., White, E., Wood, W. G., Yuan, J., Zakeri, Z., Zhivotovsky, B., Melino, G., Kroemer, G., Vitale, I., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., Calzavara Pinton, P., Galluzzi, L., Bravo-San Pedro, J. M., Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, D., Alnemri, E. S., Altucci, L., Andrews, D., Annicchiarico-Petruzzelli, M., Baehrecke, E. H., Bazan, N. G., Bertrand, M. J., Bianchi, K., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Campanella, M., Candi, E., Cecconi, F., Chan, F. K., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, A., Dawson, T. M., Dawson, V. L., De Laurenzi, V., De Maria Marchiano, Ruggero, Debatin, K. -M., Di Daniele, N., Dixit, V. M., Dynlacht, B. D., El-Deiry, W. S., Fimia, G. M., Flavell, R. A., Fulda, S., Garrido, C., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnoczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Joseph, B., Jost, P. J., Kaufmann, T., Kepp, O., Klionsky, D. J., Knight, R. A., Kumar, S., Lemasters, J. J., Levine, B., Linkermann, A., Lipton, S. A., Lockshin, R. A., López-Otín, C., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C., Martin, S. J., Martinou, J. -C., Medema, Jan Paul, Meier, P., Melino, S., Mizushima, N., Moll, U., Muñoz-Pinedo, C., Nuñez, G., Oberst, A., Panaretakis, T., Penninger, J. M., Peter, M. E., Piacentini, M., Calzavara Pinton, Piergiacomo, Prehn, J. H., Puthalakath, H., Rabinovich, G. A., Ravichandran, K. S., Rizzuto, R., Rodrigues, C. M., Rubinsztein, D. C., Rudel, T., Shi, Y., Simon, H. -U., Stockwell, B. R., Szabadkai, G., Tait, S. W., Tang, H. L., Tavernarakis, N., Tsujimoto, Y., Vanden Berghe, T., Vandenabeele, P., Villunger, A., Wagner, E. F., Walczak, H., White, E., Wood, W. G., Yuan, J., Zakeri, Z., Zhivotovsky, B., Melino, G., Kroemer, G., Vitale, I., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., and Calzavara Pinton, P.

Abstract

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). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.

Published
2015

21. NIK promotes tissue destruction independently of the alternative NF-κB pathway through TNFR1/RIP1-induced apoptosis

Author

Boutaffala, L, primary, Bertrand, M J M, additional, Remouchamps, C, additional, Seleznik, G, additional, Reisinger, F, additional, Janas, M, additional, Bénézech, C, additional, Fernandes, M T, additional, Marchetti, S, additional, Mair, F, additional, Ganeff, C, additional, Hupalowska, A, additional, Ricci, J-E, additional, Becher, B, additional, Piette, J, additional, Knolle, P, additional, Caamano, J, additional, Vandenabeele, P, additional, Heikenwalder, M, additional, and Dejardin, E, additional

Published
2015
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23. Synthesis of 2 ',3 '-cyclohexen bicyclic uridine analogues using ring-closure metathesis

Author

Drone, J., Egorov, M., Hatton, W., Bertrand, M. J., Len, C., Lebreton, J., Chimie Et Interdisciplinarité : Synthèse, Analyse, Modélisation (CEISAM), Université de Nantes - UFR des Sciences et des Techniques (UN UFR ST), and Université de Nantes (UN)-Université de Nantes (UN)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)

Abstract

0936-5214

Published
2006

25. Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Author

Galluzzi, L, primary, Bravo-San Pedro, J M, additional, Vitale, I, additional, Aaronson, S A, additional, Abrams, J M, additional, Adam, D, additional, Alnemri, E S, additional, Altucci, L, additional, Andrews, D, additional, Annicchiarico-Petruzzelli, M, additional, Baehrecke, E H, additional, Bazan, N G, additional, Bertrand, M J, additional, Bianchi, K, additional, Blagosklonny, M V, additional, Blomgren, K, additional, Borner, C, additional, Bredesen, D E, additional, Brenner, C, additional, Campanella, M, additional, Candi, E, additional, Cecconi, F, additional, Chan, F K, additional, Chandel, N S, additional, Cheng, E H, additional, Chipuk, J E, additional, Cidlowski, J A, additional, Ciechanover, A, additional, Dawson, T M, additional, Dawson, V L, additional, De Laurenzi, V, additional, De Maria, R, additional, Debatin, K-M, additional, Di Daniele, N, additional, Dixit, V M, additional, Dynlacht, B D, additional, El-Deiry, W S, additional, Fimia, G M, additional, Flavell, R A, additional, Fulda, S, additional, Garrido, C, additional, Gougeon, M-L, additional, Green, D R, additional, Gronemeyer, H, additional, Hajnoczky, G, additional, Hardwick, J M, additional, Hengartner, M O, additional, Ichijo, H, additional, Joseph, B, additional, Jost, P J, additional, Kaufmann, T, additional, Kepp, O, additional, Klionsky, D J, additional, Knight, R A, additional, Kumar, S, additional, Lemasters, J J, additional, Levine, B, additional, Linkermann, A, additional, Lipton, S A, additional, Lockshin, R A, additional, López-Otín, C, additional, Lugli, E, additional, Madeo, F, additional, Malorni, W, additional, Marine, J-C, additional, Martin, S J, additional, Martinou, J-C, additional, Medema, J P, additional, Meier, P, additional, Melino, S, additional, Mizushima, N, additional, Moll, U, additional, Muñoz-Pinedo, C, additional, Nuñez, G, additional, Oberst, A, additional, Panaretakis, T, additional, Penninger, J M, additional, Peter, M E, additional, Piacentini, M, additional, Pinton, P, additional, Prehn, J H, additional, Puthalakath, H, additional, Rabinovich, G A, additional, Ravichandran, K S, additional, Rizzuto, R, additional, Rodrigues, C M, additional, Rubinsztein, D C, additional, Rudel, T, additional, Shi, Y, additional, Simon, H-U, additional, Stockwell, B R, additional, Szabadkai, G, additional, Tait, S W, additional, Tang, H L, additional, Tavernarakis, N, additional, Tsujimoto, Y, additional, Vanden Berghe, T, additional, Vandenabeele, P, additional, Villunger, A, additional, Wagner, E F, additional, Walczak, H, additional, White, E, additional, Wood, W G, additional, Yuan, J, additional, Zakeri, Z, additional, Zhivotovsky, B, additional, Melino, G, additional, and Kroemer, G, additional

Published
2014
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26. Depletion of RIPK3 or MLKL blocks TNF-driven necroptosis and switches towards a delayed RIPK1 kinase-dependent apoptosis

Author

Remijsen, Q, primary, Goossens, V, additional, Grootjans, S, additional, Van den Haute, C, additional, Vanlangenakker, N, additional, Dondelinger, Y, additional, Roelandt, R, additional, Bruggeman, I, additional, Goncalves, A, additional, Bertrand, M J M, additional, Baekelandt, V, additional, Takahashi, N, additional, Berghe, T V, additional, and Vandenabeele, P, additional

Published
2014
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27. Loss of Maged1 results in obesity, deficits of social interactions, impaired sexual behavior and severe alteration of mature oxytocin production in the hypothalamus

Author

UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, Dombret, C., Nguyen, T., Schakman, Olivier, Michaud, J. L., Hardin-Pouzet, H., Bertrand, M. J. M., De Backer, O., UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, Dombret, C., Nguyen, T., Schakman, Olivier, Michaud, J. L., Hardin-Pouzet, H., Bertrand, M. J. M., and De Backer, O.

Abstract

MAGED1, NECDIN and MAGEL2 are members of the MAGE gene family. The latter two of these genes have been involved in Prader-Willi syndrome (PWS), which includes hyperphagia, repetitive and compulsive behaviors, and cognitive impairment. Here, we show that Maged1-deficient mice develop progressive obesity associated with hyperphagia and reduced motor activity. Loss of Maged1 also results in a complex behavioral syndrome that includes reduced social interactions and memory, deficient sexual behavior, as well as increased anxiety and self-grooming. Oxytocin (OT), which is produced in the hypothalamus, can act as a neurotransmitter that reduces anxiety, promotes social behaviors and regulates food intake. Growing evidences indicate that OT is involved in autism. We found that Maged1 mutants showed a severe reduction in the levels of mature OT, but not of its precursors, in the hypothalamus. Moreover, the administration of OT rescued the deficit in social memory of these mice. We conclude that Maged1 is required for OT processing or stability. A decrease in mature OT levels in Maged1 mutants affects social interactions and possibly other behavioral processes. Our observations suggest that, in human, MAGED1 could play a role in autism or cause a neurodevelopmental condition that is reminiscent of the PWS.

Published
2012

35. Essential versus accessory aspects of cell death: recommendations of the NCCD 2015.

Author

Galluzzi, L, Bravo-San Pedro, J M, Vitale, I, Aaronson, S A, Abrams, J M, Adam, D, Alnemri, E S, Altucci, L, Andrews, D, Annicchiarico-Petruzzelli, M, Baehrecke, E H, Bazan, N G, Bertrand, M J, Bianchi, K, Blagosklonny, M V, Blomgren, K, Borner, C, Bredesen, D E, Brenner, C, and Campanella, M

Subjects
CELL death inhibition, CELL-mediated cytotoxicity, GENETIC code, GENETIC transcription, GENETIC engineering research
Abstract

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). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death. [ABSTRACT FROM AUTHOR]

Published
2015
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45. cIAP1 and TAK1 protect cells from TNF-induced necrosis by preventing RIP1/RIP3-dependent reactive oxygen species production.

Author

Vanlangenakker, N., Vanden Berghe, T., Bogaert, P., Laukens, B., Zobel, K., Deshayes, K., Vucic, D., Fulda, S., Vandenabeele, P., and Bertrand, M. J. M.

Subjects
APOPTOSIS prevention, TRANSFORMING growth factors, ACTIVE oxygen in the body, TUMOR necrosis factors, NECROSIS
Abstract

Three members of the IAP family (X-linked inhibitor of apoptosis (XIAP), cellular inhibitor of apoptosis proteins-1/-2 (cIAP1 and cIAP2)) are potent suppressors of apoptosis. Recent studies have shown that cIAP1 and cIAP2, unlike XIAP, are not direct caspase inhibitors, but block apoptosis by functioning as E3 ligases for effector caspases and receptor-interacting protein 1 (RIP1). cIAP-mediated polyubiquitination of RIP1 allows it to bind to the pro-survival kinase transforming growth factor-β-activated kinase 1 (TAK1) which prevents it from activating caspase-8-dependent death, a process reverted by the de-ubiquitinase CYLD. RIP1 is also a regulator of necrosis, a caspase-independent type of cell death. Here, we show that cells depleted of the IAPs by treatment with the IAP antagonist BV6 are greatly sensitized to tumor necrosis factor (TNF)-induced necrosis, but not to necrotic death induced by anti-Fas, poly(I:C) oxidative stress. Specific targeting of the IAPs by RNAi revealed that repression of cIAP1 is responsible for the sensitization. Similarly, lowering TAK1 levels or inhibiting its kinase activity sensitized cells to TNF-induced necrosis, whereas repressing CYLD had the opposite effect. We show that this sensitization to death is accompanied by enhanced RIP1 kinase activity, increased recruitment of RIP1 to Fas-associated via death domain and RIP3 (which allows necrosome formation), and elevated RIP1 kinase-dependent accumulation of reactive oxygen species (ROS). In conclusion, our data indicate that cIAP1 and TAK1 protect cells from TNF-induced necrosis by preventing RIP1/RIP3-dependent ROS production. [ABSTRACT FROM AUTHOR]

Published
2011
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