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53. Transatlantic Security, Defence and Strategy: Badly Needed Reforms

Author

Peter M. E. Volten

Subjects
Politics, Social, business.industry, Political Science and International Relations, Sociology, Public administration, business, Security studies, Sosyal, Publication
Abstract

Professor Emeritus Peter Volten has been awarded Doctor Honoris Causa of the National University of Political Studies and Public Administration (May 2014) in recognition of his outstanding contribution to the field of European Security Studies. Leading author, director and editor, Prof. Volten has kindly accepted to publish his lectio prima as editorial essay in the current issue of Europolity.

Published
2014

54. Multiculturalism and Anti‐racism in a New ERA: a critical review

Author

Peter M. E. Figueroa

Subjects
Cultural Studies, Education reform, Government, Anti-racism, media_common.quotation_subject, Ethnic group, Gender studies, Racism, Education, Multiculturalism, Sociology, Social science, Philosophy of education, Demography, media_common, Diversity (politics)
Abstract

What have been the implications of the Education Reform Act 1988 and of subsequent policy developments for multicultural anti‐racist education and for educational equality for minority ethnic groups in England and Wales? Does the change of government signify a change in these regards? These issues are approached by first developing a definition of multicultural anti‐racist education on the basis of a social analysis and a social and educational philosophy. Thus, diversity, inequality and racism, and some of the evidence for them as features of British society, are briefly discussed. Next, educational policy during the last decade, its likely implications for multicultural anti‐racist education and for educational equality for minority ethnic groups, and some relevant evidence are examined. The conclusion is not only that multicultural anti‐racist education has been marginalised and minority ethnic groups poorly served educationally, but that the jury is still out with regard to the New Labour Gov...

Published
1999
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55. 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

61. Advances in apoptosis research

Author

Peter, M E, Heufelder, A E, Hengartner, M O, University of Zurich, and Peter, M E

Subjects
1000 Multidisciplinary, 570 Life sciences, biology, 10124 Institute of Molecular Life Sciences
Published
1997
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63. 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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65. Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

Author

Galluzzi, L., Aaronson, S. A., Abrams, J., Alnemri, E. S., Andrews, D. W., Baehrecke, E. H., Bazan, N. G., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Castedo, M., Cidlowski, J. A., Ciechanover, A., Cohen, G. M., De Laurenzi, V., De Maria Marchiano, Ruggero, Deshmukh, M., Dynlacht, B. D., El-Deiry, W. S., Flavell, R. A., Fulda, S., Garrido, C., Golstein, P., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnóczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Jäättelä, M., Kepp, O., Kimchi, A., Klionsky, D. J., Knight, R. A., Kornbluth, S., Kumar, S., Levine, B., Lipton, S. A., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C. W., Martin, S. J., Medema, Jan Paul, Mehlen, P., Melino, G., Moll, U. M., Morselli, E., Nagata, S., Nicholson, D. W., Nicotera, P., Nuñez, G., Oren, M., Penninger, J., Pervaiz, S., Peter, M. E., Piacentini, M., Prehn, J. H. M., Puthalakath, H., Rabinovich, G. A., Rizzuto, R., Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, T., Scorrano, L., Simon, H. -U., Steller, H., Tschopp, J., Tsujimoto, Y., Vandenabeele, P., Vitale, Ilio, Vousden, K. H., Youle, R. J., Yuan, J., Zhivotovsky, B., Kroemer, G., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., Vitale, I., Galluzzi, L., Aaronson, S. A., Abrams, J., Alnemri, E. S., Andrews, D. W., Baehrecke, E. H., Bazan, N. G., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Castedo, M., Cidlowski, J. A., Ciechanover, A., Cohen, G. M., De Laurenzi, V., De Maria Marchiano, Ruggero, Deshmukh, M., Dynlacht, B. D., El-Deiry, W. S., Flavell, R. A., Fulda, S., Garrido, C., Golstein, P., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnóczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Jäättelä, M., Kepp, O., Kimchi, A., Klionsky, D. J., Knight, R. A., Kornbluth, S., Kumar, S., Levine, B., Lipton, S. A., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C. W., Martin, S. J., Medema, Jan Paul, Mehlen, P., Melino, G., Moll, U. M., Morselli, E., Nagata, S., Nicholson, D. W., Nicotera, P., Nuñez, G., Oren, M., Penninger, J., Pervaiz, S., Peter, M. E., Piacentini, M., Prehn, J. H. M., Puthalakath, H., Rabinovich, G. A., Rizzuto, R., Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, T., Scorrano, L., Simon, H. -U., Steller, H., Tschopp, J., Tsujimoto, Y., Vandenabeele, P., Vitale, Ilio, Vousden, K. H., Youle, R. J., Yuan, J., Zhivotovsky, B., Kroemer, G., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., and Vitale, I.

Abstract

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guidelines exist regarding their use and interpretation, and nobody has thoroughly annotated the experimental settings for which each of these techniques is most appropriate. Here, we provide a nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls. These guidelines are intended for investigators who study cell death, as well as for reviewers who need to constructively critique scientific reports that deal with cellular demise. Given the difficulties in determining the exact number of cells that have passed the point-of-no-return of the signaling cascades leading to cell death, we emphasize the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells.

Published
2009

67. Establishing Security and Stability in the Wider Black Sea Area

Author

Tashev, Blagovest, Volten, Peter M. E., NATO Public Diplomacy Division, Tashev, Blagovest, Volten, Peter M. E., and NATO Public Diplomacy Division

Subjects
National security--Black Sea Region--Congresses
Abstract

'Proceedings of the NATO Advanced Research Workshop on Establishing Security and Stability in the Wider Black Sea Area: The Role of the New Democracies, Bansko, Bulgaria, 5-9 April, 2006'--T.p. verso.

Published
2007

68. Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012

Author

Galluzzi, L, primary, Vitale, I, additional, Abrams, J M, additional, Alnemri, E S, additional, Baehrecke, E H, additional, Blagosklonny, M V, additional, Dawson, T M, additional, Dawson, V L, additional, El-Deiry, W S, additional, Fulda, S, additional, Gottlieb, E, additional, Green, D R, additional, Hengartner, M O, additional, Kepp, O, additional, Knight, R A, additional, Kumar, S, additional, Lipton, S A, additional, Lu, X, additional, Madeo, F, additional, Malorni, W, additional, Mehlen, P, additional, Nuñez, G, additional, Peter, M E, additional, Piacentini, M, additional, Rubinsztein, D C, additional, Shi, Y, additional, Simon, H-U, additional, Vandenabeele, P, additional, White, E, additional, Yuan, J, additional, Zhivotovsky, B, additional, Melino, G, additional, and Kroemer, G, additional

Published
2011
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70. Low-GDP peritoneal dialysis fluid ('balance') has less impact in vitro and ex vivo on epithelial-to-mesenchymal transition (EMT) of mesothelial cells than a standard fluid

Author

Bajo, M. A., primary, Perez-Lozano, M. L., additional, Albar-Vizcaino, P., additional, del Peso, G., additional, Castro, M.-J., additional, Gonzalez-Mateo, G., additional, Fernandez-Perpen, A., additional, Aguilera, A., additional, Sanchez-Villanueva, R., additional, Sanchez-Tomero, J. A., additional, Lopez-Cabrera, M., additional, Peter, M. E., additional, Passlick-Deetjen, J., additional, and Selgas, R., additional

Published
2010
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71. Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

Author

Galluzzi, L, primary, Aaronson, S A, additional, Abrams, J, additional, Alnemri, E S, additional, Andrews, D W, additional, Baehrecke, E H, additional, Bazan, N G, additional, Blagosklonny, M V, additional, Blomgren, K, additional, Borner, C, additional, Bredesen, D E, additional, Brenner, C, additional, Castedo, M, additional, Cidlowski, J A, additional, Ciechanover, A, additional, Cohen, G M, additional, De Laurenzi, V, additional, De Maria, R, additional, Deshmukh, M, additional, Dynlacht, B D, additional, El-Deiry, W S, additional, Flavell, R A, additional, Fulda, S, additional, Garrido, C, additional, Golstein, P, additional, Gougeon, M-L, additional, Green, D R, additional, Gronemeyer, H, additional, Hajnóczky, G, additional, Hardwick, J M, additional, Hengartner, M O, additional, Ichijo, H, additional, Jäättelä, M, additional, Kepp, O, additional, Kimchi, A, additional, Klionsky, D J, additional, Knight, R A, additional, Kornbluth, S, additional, Kumar, S, additional, Levine, B, additional, Lipton, S A, additional, Lugli, E, additional, Madeo, F, additional, Malorni, W, additional, Marine, J-CW, additional, Martin, S J, additional, Medema, J P, additional, Mehlen, P, additional, Melino, G, additional, Moll, U M, additional, Morselli, E, additional, Nagata, S, additional, Nicholson, D W, additional, Nicotera, P, additional, Nuñez, G, additional, Oren, M, additional, Penninger, J, additional, Pervaiz, S, additional, Peter, M E, additional, Piacentini, M, additional, Prehn, J H M, additional, Puthalakath, H, additional, Rabinovich, G A, additional, Rizzuto, R, additional, Rodrigues, C M P, additional, Rubinsztein, D C, additional, Rudel, T, additional, Scorrano, L, additional, Simon, H-U, additional, Steller, H, additional, Tschopp, J, additional, Tsujimoto, Y, additional, Vandenabeele, P, additional, Vitale, I, additional, Vousden, K H, additional, Youle, R J, additional, Yuan, J, additional, Zhivotovsky, B, additional, and Kroemer, G, additional

Published
2009
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73. Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009

Author

Kroemer, G, primary, Galluzzi, L, additional, Vandenabeele, P, additional, Abrams, J, additional, Alnemri, E S, additional, Baehrecke, E H, additional, Blagosklonny, M V, additional, El-Deiry, W S, additional, Golstein, P, additional, Green, D R, additional, Hengartner, M, additional, Knight, R A, additional, Kumar, S, additional, Lipton, S A, additional, Malorni, W, additional, Nuñez, G, additional, Peter, M E, additional, Tschopp, J, additional, Yuan, J, additional, Piacentini, M, additional, Zhivotovsky, B, additional, and Melino, G, additional

Published
2008
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74. Expression of c-FLIP(L) and resistance to CD95-mediated apoptosis of monocyte-derived dendritic cells: inhibition by bisindolylmaleimide.

Author

Willems, Fabienne, Amraoui, Z, Vanderheyde, N, Verhasselt, Valérie, Aksoy, Ezra, Scaffidi, C., Peter, M E, Krammer, P., Goldman, Michel, Willems, Fabienne, Amraoui, Z, Vanderheyde, N, Verhasselt, Valérie, Aksoy, Ezra, Scaffidi, C., Peter, M E, Krammer, P., and Goldman, Michel

Abstract

To gain insight into the mechanisms controlling apoptosis of dendritic cells (DC), human monocyte-derived DC were analyzed for their expression of CD95 (Fas/Apo-1) and their response to CD95 ligation. Although DC expressed the CD95 molecule on their membrane, they did not undergo apoptosis on CD95 ligation unless sensitized by cycloheximide. In parallel, DC synthesized c-FLIP(L), an inhibitor of the CD95-mediated death-signaling cascade. We also demonstrated that bisindolylmaleimide down-regulates c-FLIP(L) expression in DC and, in parallel, allows CD95-mediated apoptosis in these cells. In contrast, Bcl-2, Bcl-x(L), and Bax levels were not affected by bisindolylmaleimide. We conclude that DC resist CD95- mediated apoptosis in association with c-FLIP(L) expression and that the immunosuppressive potential of bisindolylmaleimide previously observed at the T-cell level also involves facilitation of CD95-mediated DC apoptosis., Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2000

77. Apoptosis signaling by death receptors

Author

Schulze-Osthoff, Klaus, Ferrari, D., Los, Marek Jan, Wesselborg, Sebastian, Peter, M. E., Schulze-Osthoff, Klaus, Ferrari, D., Los, Marek Jan, Wesselborg, Sebastian, and Peter, M. E.

Abstract

Death receptors have been recently identified as a subgroup of the TNF-receptor superfamily with a predominant function in induction of apoptosis. The receptors are characterized by an intracellular region, called the death domain, which is required for the transmission of the cytotoxic signal. Currently, five different such death receptors are known including tumor necrosis factor (TNF) receptor-1, CD95 (Fas/APO-1), TNF-receptor-related apoptosis-mediated protein (TRAMP) and TNF-related apoptosis-inducing ligand (TRAIL) receptor-1 and -2. The signaling pathways by which these receptors induce apoptosis are rather similar. Ligand binding induces receptor oligomerization, followed by the recruitment of an adaptor protein to the death domain through homophilic interaction. The adaptor protein then binds a proximal caspase, thereby connecting receptor signaling to the apoptotic effector machinery. In addition, further pathways have been linked to death receptor-mediated apoptosis, such as sphingomyelinases, JNK kinases and oxidative stress. These pro-apoptotic signals are counteracted by several mechanisms which inhibit apoptosis at different levels. This review summarizes the current and rapidly expanding knowledge about the biological functions of death receptors and the mechanisms to trigger or to counteract cell death.

Published
1998
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79. Betulinic acid triggers CD95 (APO-1/Fas)- and p53-independent apoptosis via activation of caspases in neuroectodermal tumors

Author

Fulda, S., Friesen, C., Los, Marek Jan, Scaffidi, C., Mier, W., Benedict, M., Nunez, G., Krammer, P. H., Peter, M. E., Debatin, K. M., Fulda, S., Friesen, C., Los, Marek Jan, Scaffidi, C., Mier, W., Benedict, M., Nunez, G., Krammer, P. H., Peter, M. E., and Debatin, K. M.

Abstract

Betulinic acid CBA), a melanoma-specific cytotoxic agent, induced apoptosis in neuroectodermal tumors, such as neuroblastoma, medulloblastoma, and Ewing's sarcoma, representing the most common solid tumors of childhood. BA triggered an apoptosis pathway different from the one previously identified for standard chemotherapeutic drugs. BA-induced apoptosis was independent of CD95-ligand/receptor interaction and accumulation of wild-type p53 protein, but it critically depended on activation of caspases (interleukin 1 beta-converting enzyme/Ced-3-like proteases), FLICE/MACH (caspase-8), considered to be an upstream protease in the caspase cascade, and the downstream caspase CPP32/YAMA/Apopain (caspase-3) were activated, resulting in cleavage of the prototype substrate of caspases PARP. The broad-spectrum peptide inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, which blocked cleavage of FLICE and PARP, also completely abrogated BA-triggered apoptosis. Cleavage of caspases was preceded by disturbance of mitochondrial membrane potential and by generation of reactive oxygen species. Overexpression of Bcl-2 and Bcl-x(L) conferred resistance to BA at the level of mitochondrial dysfunction, protease activation, and nuclear fragmentation. This suggested that mitochondrial alterations were involved in BA-induced activation of caspases. Furthermore, pax and Bcl-x(s), two death-promoting proteins of the Bcl-2 family, were up-regulated following BA treatment. Most importantly, neuroblastoma cells resistant to CD95- and doxorubicin-mediated apoptosis were sensitive to treatment with BA, suggesting that BA may bypass some forms of drug resistance. Because BA exhibited significant antitumor activity on patients' derived neuroblastoma cells ex vivo, BA may be a promising new agent for the treatment of neuroectodermal tumors in vivo.

Published
1997

81. International Relations, Political Culture, and Security: Conceptual Challenges.

Author

Volten, Peter M. E. and Tashev, Blagovest

Abstract

The article explores the security challenges facing countries in the Wider Black Sea Area (WBSA) in relation to international politics (IP) and international relations (IR). A definition of strategy is given, along with its political dimension. Particular focus is given to the extent to which American IR differs from that of other countries and the interaction between politics and political culture. Also included are the European Union's (EU) security approach to WBSA, key elements for understanding security, barriers to regional security cooperation.

Published
2007

82. Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor

Author

Kischkel, F. C., Hellbardt, S., Behrmann, Iris, Germer, M., Pawlita, M., Krammer, P. H., Peter, M. E., Kischkel, F. C., Hellbardt, S., Behrmann, Iris, Germer, M., Pawlita, M., Krammer, P. H., and Peter, M. E.

Abstract

APO-1 (Fas/CD95), a member of the tumor necrosis factor receptor superfamily, induces apoptosis upon receptor oligomerization. In a search to identify intracellular signaling molecules coupling to oligomerized APO-1, several cytotoxicity-dependent APO-1-associated proteins (CAP) were immunoprecipitated from the apoptosis-sensitive human leukemic T cell line HUT78 and the lymphoblastoid B cell line SKW6.4. CAP1-3 (27-29 kDa) and CAP4 (55 kDa), instantly detectable after the crosslinking of APO-1, were associated only with aggregated (the signaling form of APO-1) and not with monomeric APO-1. CAP1 and CAP2 were identified as serine phosphorylated MORT1/FADD. The association of CAP1-4 with APO-1 was not observed with C-terminally truncated non-signaling APO-1. In addition, CAP1 and CAP2 did not associate with an APO-1 cytoplasmic tail carrying the lprcg amino acid replacement. Moreover, no APO-1-CAP association was found in the APO-1+, anti-APO-1-resistant pre-B cell line Boe. Our data suggest that in vivo CAP1-4 are the APO-1 apoptosis-transducing molecules.

Published
1996
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86. TRANSATLANTIC SECURITY, DEFENCE AND STRATEGY: BADLY NEEDED REFORMS.

Author

VOLTEN, Peter M. E.

Subjects
AUTHORS, POLITICAL leadership, MILITARY strategy
Abstract

Professor Emeritus Peter Volten has been awarded Doctor Honoris Causa of the National University of Political Studies and Public Administration (May 2014) in recognition of his outstanding contribution to the field of European Security Studies. Leading author, director and editor, Prof. Volten has kindly accepted to publish his lectio prima as editorial essay in the current issue of Europolity. [ABSTRACT FROM AUTHOR]

Published
2014

91. Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009.

Author

Kroemer, G., Galluzzi, L., Vandenabeele, P., Abrams, J., Alnemri, E. S., Baehrecke, E. H., Blagosklonny, M. V., El-Deiry, W. S., Golstein, P., Green, D. R., Hengartner, M., Knight, R. A., Kumar, S., Lipton, S. A., Malorni, W., Nuñez, G., Peter, M. E., Tschopp, J., Yuan, J., and Piacentini, M.

Subjects
CELL death, BIOCHEMISTRY, APOPTOSIS, NECROSIS, AUTOPHAGY, CELLULAR mechanics
Abstract

Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like ‘percentage apoptosis’ and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that ‘autophagic cell death’ is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including ‘entosis’, ‘mitotic catastrophe’, ‘necrosis’, ‘necroptosis’ and ‘pyroptosis’.Cell Death and Differentiation (2009) 16, 3–11; doi:10.1038/cdd.2008.150; published online 10 October 2008 [ABSTRACT FROM AUTHOR]

Published
2009
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92. CD95 apoptosis resistance in certain cells can be overcome by noncanonical activation of caspase-8.

Author

Barnhart, B. C., Pietras, E. M., Algeciras-Schimnich, A., Salmena, L., Sayama, K., Hakem, R., and Peter, M. E.

Subjects
APOPTOSIS, CELLS, TUMORS, CELLULAR pathology, CANCER cells, GENETIC mutation
Abstract

CD95 apoptosis resistance of tumor cells is often acquired through mutations in the death domain (DD) of one of the CD95 alleles. Furthermore, Type I cancer cells are resistant to induction of apoptosis by soluble CD95 ligand (CD95L), which does not induce efficient formation of the death-inducing signaling complex (DISC). Here, we report that tumor cells expressing a CD95 allele that lacks a functional DD, splenocytes from heterozygous lprcg mice, which express one mutated CD95 allele, and Type I tumor cells stimulated with soluble CD95L can all die through CD95 when protein synthesis or nuclear factor kappa B is inhibited. This noncanonical form of CD95-mediated apoptosis is dependent on the enzymatic activity of procaspase-8 but does not involve fully processed active caspase-8 subunits. Our data suggest that it is possible to overcome the CD95 apoptosis resistance of many tumor cells that do not efficiently form a DISC through noncanonical activation of the caspase-8 proenzyme.Cell Death and Differentiation (2005) 12, 25-37. doi:10.1038/sj.cdd.4401509 Published online 22 October 2004 [ABSTRACT FROM AUTHOR]

Published
2005
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94. Teachers’ and pupils’ racist and ethnocentric frames of reference: A case study

Author

L. Thomas Swart and Peter M. E. Figueroa

Subjects
Ethnocentrism, Geography, Planning and Development, Pedagogy, General Earth and Planetary Sciences, General Medicine, Sociology, Frame of reference, General Environmental Science
Abstract

(1986). Teachers’ and pupils’ racist and ethnocentric frames of reference: A case study. New Community: Vol. 13, No. 1, pp. 40-51.

Published
1986
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95. Reviews

Author

Ian Lister, Kevin Durkin, Peter M. E. Figueroa, Monica J. Taylor, J. P. Tuck, Leslie R. Perry, J. H. Higginson, Tessa Blackstone, Beryl Madoc‐Jones, W. Gareth Evans, and Kenneth Smart

Subjects
Education
Published
1979
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96. Books

Author

Louis James, Wilson Harris, Vaughan Robinson, John Solomos, R. A. B. Leaper, Peter Shipley, Michael Billig, Raymond Cochrane, and Peter M. E. Figueroa

Subjects
Arts and Humanities (miscellaneous), Demography
Published
1982
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97. The death effector domain-associated factor plays distinct regulatory roles in the nucleus and cytoplasm.

Author

Zheng, L, Schickling, O, Peter, M E, and Lenardo, M J

Abstract

Homophilic interactions of death effector domains (DEDs) are crucial for the signaling pathways of death receptor-mediated apoptosis. The machinery that regulates proper oligomerization and autoactivation of procaspase-8 and/or procaspase-10 during T lymphocyte activation determines whether the cells will undergo caspase-mediated apoptosis or proliferation. We screened a yeast two-hybrid library by using the DEDs contained in the prodomains of procaspase-8 and procaspase-10 and isolated a DED-associated factor (DEDAF) that interacts with several DED-containing proteins but does not itself contain a DED. DEDAF is highly conserved between human and mouse (98% amino acid identity) and is homologous to a nuclear regulatory protein YAF-2. DEDAF is expressed at the highest levels in lymphoid tissues and placenta. DEDAF interacts with FADD, procaspase-8, and procaspase-10 in the cytosol as well as with the DED-containing DNA-binding protein (DEDD) in the nucleus. At the cell membrane, DEDAF augmented the formation of CD95-FADD-caspase-8 complexes and enhanced death receptor- as well as DED-mediated apoptosis. In the nucleus, DEDAF caused the DEDD protein to relocalize from subnuclear structures to a diffuse distribution in the nucleoplasm. Our data therefore suggest that DEDAF may be involved in the regulation of both cytoplasmic and nuclear events of apoptosis.

Published
2001
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98. Differential modulation of apoptosis sensitivity in CD95 type I and type II cells.

Author

Scaffidi, C, Schmitz, I, Zha, J, Korsmeyer, S J, Krammer, P H, and Peter, M E

Abstract

We have recently identified two different pathways of CD95-mediated apoptosis (Scaffidi, C., Fulda, S., Srinivasan, A., Feng, L., Friesen, C., Tomaselli, K. J., Debatin, K.-M., Krammer, P. H., and Peter, M. E. (1998) EMBO J. 17, 1675-1687). CD95-mediated apoptosis in type I cells is initiated by large amounts of active caspase-8 formed at the death-inducing signaling complex (DISC) followed by direct cleavage of caspase-3. In contrast, in type II cells very little DISC and small amounts of active caspase-8 sufficient to induce the apoptogenic activity of mitochondria are formed causing a profound activation of both caspase-8 and caspase-3. Only in type II cells can apoptosis be blocked by overexpressed Bcl-2 or Bcl-x(L). We now show that a number of apoptosis-inhibiting or -inducing stimuli only affect apoptosis in type II cells, indicating that they act on the mitochondrial branch of the CD95 pathway. These stimuli include the activation of protein kinase C, which inhibits CD95-mediated apoptosis resulting in a delayed cleavage of BID, and the induction of apoptosis by the ceramide analog C(2)-ceramide. In addition, we have identified the CD95 high expressing cell line Boe(R) as a CD95 apoptosis-resistant type II cell that can be sensitized by treatment with cycloheximide without affecting formation of the DISC. This also places the effects of cycloheximide in the mitochondrial branch of the type II CD95 pathway. In contrast, c-FLIP was found to block CD95-mediated apoptosis in both type I and type II cells, because it acts directly at the DISC of both types of cells.

Published
1999

99. The role of c-FLIP in modulation of CD95-induced apoptosis.

Author

Scaffidi, C, Schmitz, I, Krammer, P H, and Peter, M E

Abstract

Upon stimulation, CD95 (APO-1/Fas) recruits the adapter molecule Fas-associated death domain protein (FADD)/MORT1 and caspase-8 (FADD-like interleukin-1beta-converting enzyme (FLICE)/MACH/MCH5) into the death-inducing signaling complex (DISC). Recently, a molecule with sequence homology to caspase-8 was identified, termed cellular FLICE-inhibitory protein (c-FLIP). c-FLIP has been controversially reported to possess apoptosis-promoting and -inhibiting functions. Using c-FLIP-specific monoclonal antibodies, we now show that c-FLIP is expressed in two isoforms, both of which, like FADD and caspase-8, are recruited to the CD95 DISC in a stimulation-dependent fashion. In stably transfected BJAB cells, c-FLIP blocks caspase-8 activation at the DISC and thereby inhibits CD95-mediated apoptosis. During this process, both caspase-8 and c-FLIP undergo cleavage between the p18 and p10 subunits, generating two stable intermediates of 43 kDa that stay bound to the DISC. c-FLIP has been suggested to play a role in protecting activated peripheral T cells from CD95-mediated apoptosis (Irmler, M., Thome, M., Hahne, M., Schneider, P., Hofmann, K., Steiner, V., Bodmer, J. L. , Schroter, M., Burns, K., Mattmann, C., Rimoldi, D., French, L. E., and Tschopp, J. (1997) Nature 388, 190-195). In contrast to this hypothesis, neither caspase-8 nor c-FLIP were cleaved in these cells, ruling out c-FLIP as the main factor regulating DISC activity. Moreover, recruitment of FADD, caspase-8, and c-FLIP to the DISC was strongly reduced in the apoptosis-resistant but readily detectable in the apoptosis-sensitive T cells.

Published
1999

100. Bcl-xL acts downstream of caspase-8 activation by the CD95 death-inducing signaling complex.

Author

Medema, J P, Scaffidi, C, Krammer, P H, and Peter, M E

Abstract

The Bcl-2 family member Bcl-xL has often been correlated with apoptosis resistance. We have shown recently that in peripheral human T cells resistance to CD95-mediated apoptosis is characterized by a lack of caspase-8 recruitment to the CD95 death-inducing signaling complex (DISC) and by increased expression of Bcl-xL (Peter, M. E., Kischkel, F. C., Scheuerpflug, C. G., Medema, J. P., Debatin, K.-M., and Krammer, P. H. (1997) Eur. J. Immunol. 27, 1207-1212). This raises the possibility that Bcl-xL directly prevents caspase-8 activation by the DISC. To test this hypothesis a cell line in which CD95 signaling was inhibited by overexpression of Bcl-xL was used. In these MCF7-Fas-bcl-xL cells Bcl-xL had no effect on the recruitment of caspase-8 to the DISC. It did not affect the activity of the DISC nor the generation of the caspase-8 active subunits p18 and p10. In contrast, cleavage of a typical substrate for caspase-3-like proteases, poly(ADP-ribose) polymerase, was inhibited in comparison with the control-transfected CD95-sensitive MCF7-Fas cells. To test whether Bcl-xL would inhibit active caspase-8 subunits in the cytoplasm, a number of immunoprecipitation experiments were performed. Using monoclonal antibodies directed against different domains of caspase-8, anti-Bcl-xL antibodies, or fusion proteins of glutathione S-transferase with different domains of caspase-8, no evidence for a direct or indirect physical interaction between caspase-8 and Bcl-xL was found. Moreover, overexpression of Bcl-xL did not inhibit the activity of the caspase-8 active subunits p18/p10. Therefore, in this cell line that has become resistant to CD95-induced apoptosis due to overexpression of Bcl-xL, Bcl-xL acts independently and downstream of caspase-8.

Published
1998

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