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187 results on '"Bianchi, MARCO EMILIO"'

1. The acidic intrinsically disordered region of the inflammatory mediator HMGB1 mediates fuzzy interactions with CXCL12

Author

Mantonico, Malisa Vittoria, De Leo, Federica, Quilici, Giacomo, Colley, Liam Sean, De Marchis, Francesco, Crippa, Massimo, Mezzapelle, Rosanna, Schulte, Tim, Zucchelli, Chiara, Pastorello, Chiara, Carmeno, Camilla, Caprioglio, Francesca, Ricagno, Stefano, Giachin, Gabriele, Ghitti, Michela, Bianchi, Marco Emilio, and Musco, Giovanna

Published
2024
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3. 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. Marie [0000-0002-4847-2045], Haupt, Ygal [0000-0001-5925-0096], He, Sudan [0000-0002-0846-1210], Heery, David M. [0000-0002-5035-2392], Hengartner, Michael O. [0000-0002-7584-596X], Hetz, Claudio [0000-0003-1120-7966], Hildeman, David A. [0000-0002-0421-8483], Ichijo, Hidenori [0000-0002-5005-6438], Jäättelä, Marja [0000-0001-5950-7111], Janic, Ana [0000-0002-4200-2560], Joseph, Bertrand [0000-0001-5655-9979], Jost, Philipp J. [0000-0003-2454-0362], Kanneganti, Thirumala-Devi [0000-0002-6395-6443], Karin, Michael [0000-0002-2758-6473], Kashkar, Hamid [0000-0003-2796-1429], Kaufmann, Thomas [0000-0001-9906-874X], Kelly, Gemma L. [0000-0002-6533-1201], Kepp, Oliver [0000-0002-6081-9558], Kimchi, Adi [0000-0002-8236-8989], Klionsky, Daniel J. [0000-0002-7828-8118], Kluck, Ruth [0000-0002-7101-1925], Krysko, Dmitri V. [0000-0002-9692-2047], Kulms, Dagmar [0000-0001-6874-0548], Kumar, Sharad [0000-0001-7126-9814], Lavandero, Sergio [0000-0003-4258-1483], Lavrik, Inna N. [0000-0002-9324-309X], Liccardi, Gianmaria [0000-0002-2662-1281], Linkermann, Andreas [0000-0001-6287-9725], Lipton, Stuart A. [0000-0002-3490-1259], Lockshin, Richard A. [0000-0002-4389-4898], López-Otín, Carlos [0000-0001-6964-1904], Luedde, Tom [0000-0002-6288-8821], MacFarlane, Marion [0000-0001-7886-1159], Madeo, Frank [0000-0002-5070-1329], Malorni, Walter [0000-0002-1223-7000], Manic, Gwenola [0000-0003-3759-8029], Marchi, Saverio [0000-0003-2708-1843], Marine, Jean-Christophe [0000-0003-2433-9837], Martin, Seamus J. [0000-0002-8539-3143], Martinou, Jean-Claude [0000-0002-9847-2051], Mastroberardino, Pier G. [0000-0003-2364-4258], Medema, Jan Paul [0000-0003-3045-2924], Mehlen, Patrick [0000-0003-1743-5417], Meier, Pascal [0000-0003-2760-6523], Melino, Gerry [0000-0001-9428-5972], Melino, Sonia [0000-0001-7694-5279], Miao, Edward A. [0000-0001-7295-3490], Moll, Ute M. [0000-0003-1908-7516], Muñoz-Pinedo, Cristina [0000-0002-9120-664X], Murphy, Daniel J. [0000-0002-5538-5468], Niklison-Chirou, Maria Victoria [0000-0002-2147-370X], Novelli, Flavia [0000-0002-3746-7478], Oberst, Andrew [0000-0002-9500-7912], Ofengeim, Dimitry [0000-0003-2348-3642], Opferman, Joseph T. [0000-0002-1147-5621], Oren, Moshe [0000-0003-4311-7172], Pagano, Michele [0000-0003-3210-2442], Panaretakis, Theocharis [0000-0001-5754-6950], Pasparakis, Manolis [0000-0002-9870-0966], Penninger, Josef M. [0000-0002-8194-3777], Pentimalli, Francesca [0000-0003-4740-6801], Pereira, David M. [0000-0003-0384-7592], Pervaiz, Shazib [0000-0002-4738-019X], Peter, Marcus E. [0000-0003-3216-036X], Pinton, Paolo [0000-0001-7108-6508], Porta, Giovanni [0000-0001-5260-2415], Puthalakath, Hamsa [0000-0001-5178-1175], Rabinovich, Gabriel A. [0000-0002-0947-8735], Rajalingam, Krishnaraj [0000-0002-4175-9633], Ravinchandran, Kodi S. [0000-0001-9049-1410], Rehm, Markus [0000-0001-6149-9261], Ricci, Jean-Ehrland [0000-0003-1585-8117], Rizzuto, Rosario [0000-0001-7044-5097], Robinson, Nirmal [0000-0002-7361-9491], Rotblat, Barak [0000-0003-2985-7115], Rothlin, Carla V. [0000-0002-5693-5572], Rubinsztein, David C. [0000-0001-5002-5263], Rufini, Alessandro [0000-0002-5855-655X], Ryan, Kevin M. [0000-0002-1059-9681], Sarosiek, Kristopher A. [0000-0002-4618-5085], Sawa, Akira [0000-0003-1401-3008], Sayan, Emre [0000-0002-5291-1485], Schroder, Kate [0000-0001-9261-3805], Scorrano, Luca [0000-0002-8515-8928], Sesti, Federico [0000-0002-2761-9693], Shi, Yufang [0000-0001-8964-319X], Sica, Giuseppe [0000-0002-7407-0584], Silke, John [0000-0002-7611-5774], Simon, Hans-Uwe [0000-0002-9404-7736], Sistigu, Antonella [0000-0002-2528-1238], Stockwell, Brent R. [0000-0002-3532-3868], Strappazzon, Flavie [0000-0003-0285-7449], Sun, Liming [0000-0002-0136-5605], Sun, Erwei [0000-0001-5664-513X], Szabadkai, G [0000-0002-3006-3577], Tait, Stephen W. G. [0000-0001-7697-132X], Tang, Daolin [0000-0002-1903-6180], Tavernarakis, Nektarios [0000-0002-5253-1466], Turk, Boris [0000-0002-9007-5764], Urbano, Nicoletta [0000-0003-1822-155X], Vandenabeele, Peter [0000-0002-6669-8822], Vanden Berghe, Tom [0000-0002-1633-0974], Vander Heiden, Matthew G. [0000-0002-6702-4192], Vanderluit, Jacqueline L. [0000-0002-4960-920X], Verkhratsky, A. [0000-0003-2592-9898], Villunger, Andreas [0000-0001-8259-4153], Von Karstedt, Silvia [0000-0002-7816-5919], Voss, Anne K. [0000-0002-3853-9381], Vucic, Domagoj [0000-0003-3614-8093], Vuri, Daniela [0000-0001-8693-3845], Wagner, Erwin F. [0000-0001-7872-0196], Walczak, Henning [0000-0002-6312-4591], Wallach, David [0000-0003-2724-9757], Wang, Ruoning [0000-0001-9798-8032], Weber, Achim [0000-0003-0073-3637], Yamazaki, Takahiro [0000-0002-7420-4394], Zakeri, Zahra [0000-0003-4386-8072], Zawacka-Pankau, Joanna E. [0000-0002-7415-2942], Zhivotovsky, Boris [0000-0002-2238-3482], Piacentini, Mauro [0000-0003-2919-1296], Kroemer, Guido [0000-0002-9334-4405], Galluzzi, Lorenzo [0000-0003-2257-8500 ], Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Dieter, Adam, 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 J. M., Bianchi, Marco Emilio, Blagosklonny, Mikhail V., Blander, J. 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, Galluzzi, Lorenzo, 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. Marie [0000-0002-4847-2045], Haupt, Ygal [0000-0001-5925-0096], He, Sudan [0000-0002-0846-1210], Heery, David M. [0000-0002-5035-2392], Hengartner, Michael O. [0000-0002-7584-596X], Hetz, Claudio [0000-0003-1120-7966], Hildeman, David A. [0000-0002-0421-8483], Ichijo, Hidenori [0000-0002-5005-6438], Jäättelä, Marja [0000-0001-5950-7111], Janic, Ana [0000-0002-4200-2560], Joseph, Bertrand [0000-0001-5655-9979], Jost, Philipp J. [0000-0003-2454-0362], Kanneganti, Thirumala-Devi [0000-0002-6395-6443], Karin, Michael [0000-0002-2758-6473], Kashkar, Hamid [0000-0003-2796-1429], Kaufmann, Thomas [0000-0001-9906-874X], Kelly, Gemma L. [0000-0002-6533-1201], Kepp, Oliver [0000-0002-6081-9558], Kimchi, Adi [0000-0002-8236-8989], Klionsky, Daniel J. [0000-0002-7828-8118], Kluck, Ruth [0000-0002-7101-1925], Krysko, Dmitri V. [0000-0002-9692-2047], Kulms, Dagmar [0000-0001-6874-0548], Kumar, Sharad [0000-0001-7126-9814], Lavandero, Sergio [0000-0003-4258-1483], Lavrik, Inna N. [0000-0002-9324-309X], Liccardi, Gianmaria [0000-0002-2662-1281], Linkermann, Andreas [0000-0001-6287-9725], Lipton, Stuart A. [0000-0002-3490-1259], Lockshin, Richard A. [0000-0002-4389-4898], López-Otín, Carlos [0000-0001-6964-1904], Luedde, Tom [0000-0002-6288-8821], MacFarlane, Marion [0000-0001-7886-1159], Madeo, Frank [0000-0002-5070-1329], Malorni, Walter [0000-0002-1223-7000], Manic, Gwenola [0000-0003-3759-8029], Marchi, Saverio [0000-0003-2708-1843], Marine, Jean-Christophe [0000-0003-2433-9837], Martin, Seamus J. [0000-0002-8539-3143], Martinou, Jean-Claude [0000-0002-9847-2051], Mastroberardino, Pier G. [0000-0003-2364-4258], Medema, Jan Paul [0000-0003-3045-2924], Mehlen, Patrick [0000-0003-1743-5417], Meier, Pascal [0000-0003-2760-6523], Melino, Gerry [0000-0001-9428-5972], Melino, Sonia [0000-0001-7694-5279], Miao, Edward A. [0000-0001-7295-3490], Moll, Ute M. [0000-0003-1908-7516], Muñoz-Pinedo, Cristina [0000-0002-9120-664X], Murphy, Daniel J. [0000-0002-5538-5468], Niklison-Chirou, Maria Victoria [0000-0002-2147-370X], Novelli, Flavia [0000-0002-3746-7478], Oberst, Andrew [0000-0002-9500-7912], Ofengeim, Dimitry [0000-0003-2348-3642], Opferman, Joseph T. [0000-0002-1147-5621], Oren, Moshe [0000-0003-4311-7172], Pagano, Michele [0000-0003-3210-2442], Panaretakis, Theocharis [0000-0001-5754-6950], Pasparakis, Manolis [0000-0002-9870-0966], Penninger, Josef M. [0000-0002-8194-3777], Pentimalli, Francesca [0000-0003-4740-6801], Pereira, David M. [0000-0003-0384-7592], Pervaiz, Shazib [0000-0002-4738-019X], Peter, Marcus E. [0000-0003-3216-036X], Pinton, Paolo [0000-0001-7108-6508], Porta, Giovanni [0000-0001-5260-2415], Puthalakath, Hamsa [0000-0001-5178-1175], Rabinovich, Gabriel A. [0000-0002-0947-8735], Rajalingam, Krishnaraj [0000-0002-4175-9633], Ravinchandran, Kodi S. [0000-0001-9049-1410], Rehm, Markus [0000-0001-6149-9261], Ricci, Jean-Ehrland [0000-0003-1585-8117], Rizzuto, Rosario [0000-0001-7044-5097], Robinson, Nirmal [0000-0002-7361-9491], Rotblat, Barak [0000-0003-2985-7115], Rothlin, Carla V. [0000-0002-5693-5572], Rubinsztein, David C. [0000-0001-5002-5263], Rufini, Alessandro [0000-0002-5855-655X], Ryan, Kevin M. [0000-0002-1059-9681], Sarosiek, Kristopher A. [0000-0002-4618-5085], Sawa, Akira [0000-0003-1401-3008], Sayan, Emre [0000-0002-5291-1485], Schroder, Kate [0000-0001-9261-3805], Scorrano, Luca [0000-0002-8515-8928], Sesti, Federico [0000-0002-2761-9693], Shi, Yufang [0000-0001-8964-319X], Sica, Giuseppe [0000-0002-7407-0584], Silke, John [0000-0002-7611-5774], Simon, Hans-Uwe [0000-0002-9404-7736], Sistigu, Antonella [0000-0002-2528-1238], Stockwell, Brent R. [0000-0002-3532-3868], Strappazzon, Flavie [0000-0003-0285-7449], Sun, Liming [0000-0002-0136-5605], Sun, Erwei [0000-0001-5664-513X], Szabadkai, G [0000-0002-3006-3577], Tait, Stephen W. G. [0000-0001-7697-132X], Tang, Daolin [0000-0002-1903-6180], Tavernarakis, Nektarios [0000-0002-5253-1466], Turk, Boris [0000-0002-9007-5764], Urbano, Nicoletta [0000-0003-1822-155X], Vandenabeele, Peter [0000-0002-6669-8822], Vanden Berghe, Tom [0000-0002-1633-0974], Vander Heiden, Matthew G. [0000-0002-6702-4192], Vanderluit, Jacqueline L. [0000-0002-4960-920X], Verkhratsky, A. [0000-0003-2592-9898], Villunger, Andreas [0000-0001-8259-4153], Von Karstedt, Silvia [0000-0002-7816-5919], Voss, Anne K. [0000-0002-3853-9381], Vucic, Domagoj [0000-0003-3614-8093], Vuri, Daniela [0000-0001-8693-3845], Wagner, Erwin F. [0000-0001-7872-0196], Walczak, Henning [0000-0002-6312-4591], Wallach, David [0000-0003-2724-9757], Wang, Ruoning [0000-0001-9798-8032], Weber, Achim [0000-0003-0073-3637], Yamazaki, Takahiro [0000-0002-7420-4394], Zakeri, Zahra [0000-0003-4386-8072], Zawacka-Pankau, Joanna E. [0000-0002-7415-2942], Zhivotovsky, Boris [0000-0002-2238-3482], Piacentini, Mauro [0000-0003-2919-1296], Kroemer, Guido [0000-0002-9334-4405], Galluzzi, Lorenzo [0000-0003-2257-8500 ], Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Dieter, Adam, 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 J. M., Bianchi, Marco Emilio, Blagosklonny, Mikhail V., Blander, J. 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

5. Heparin Protects Human Neural Progenitor Cells from Zika Virus-Induced Cell Death While Preserving Their Differentiation into Mature Neuroglial Cells

Author

Pagani, Isabel, primary, Ottoboni, Linda, additional, Podini, Paola, additional, Ghezzi, Silvia, additional, Brambilla, Elena, additional, Bezukladova, Svetlana, additional, Corti, Davide, additional, Bianchi, Marco Emilio, additional, Capobianchi, Maria Rosaria, additional, Poli, Guido, additional, Panina-Bordignon, Paola, additional, Yates, Edwin A., additional, Martino, Gianvito, additional, and Vicenzi, Elisa, additional

Published
2022
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6. Pamoic acid is an inhibitor of HMGB1•CXCL12 elicited chemotaxis and reduces inflammation in murine models of Pseudomonas aeruginosa pneumonia

Author

De Leo, Federica, primary, Rossi, Alice, additional, De Marchis, Francesco, additional, Cigana, Cristina, additional, Melessike, Medede, additional, Quilici, Giacomo, additional, De Fino, Ida, additional, Mantonico, Malisa Vittoria, additional, Fabris, Chantal, additional, Bragonzi, Alessandra, additional, Bianchi, Marco Emilio, additional, and Musco, Giovanna, additional

Published
2022
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7. Additional file 1 of Pamoic acid is an inhibitor of HMGB1·CXCL12 elicited chemotaxis and reduces inflammation in murine models of Pseudomonas aeruginosa pneumonia

Author

De Leo, Federica, Rossi, Alice, De Marchis, Francesco, Cigana, Cristina, Melessike, Medede, Quilici, Giacomo, De Fino, Ida, Mantonico, Malisa Vittoria, Fabris, Chantal, Bragonzi, Alessandra, Bianchi, Marco Emilio, and Musco, Giovanna

Abstract

Additional file 1. Supplementary Methods (NMR measurements; Data Driven Docking Models and molecular images; Mouse Model; Bacteria preparation for acute infection; Agar beads preparation for chronic infection; Mice treatment with PAM), Supplementary Figures S1–S11 and Supplementary Tables S1–S2.

Published
2022
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8. Rebalancing expression of HMGB1 redox isoforms to counteract muscular dystrophy

Author

Careccia, G, Saclier, M, Tirone, M, Ruggieri, E, Principi, E, Raffaghello, L, Torchio, S, Recchia, D, Canepari, M, Gorzanelli, A, Ferrara, M, Castellani, P, Rubartelli, A, Rovere-Querini, P, Casalgrandi, M, Preti, A, Lorenzetti, I, Bruno, C, Bottinelli, R, Brunelli, S, Previtali, S, Bianchi, M, Messina, G, Vénéreau, E, Careccia, Giorgia, Saclier, Marielle, Tirone, Mario, Ruggieri, Elena, Principi, Elisa, Raffaghello, Lizzia, Torchio, Silvia, Recchia, Deborah, Canepari, Monica, Gorzanelli, Andrea, Ferrara, Michele, Castellani, Patrizia, Rubartelli, Anna, Rovere-Querini, Patrizia, Casalgrandi, Maura, Preti, Alessandro, Lorenzetti, Isabella, Bruno, Claudio, Bottinelli, Roberto, Brunelli, Silvia, Previtali, Stefano Carlo, Bianchi, Marco Emilio, Messina, Graziella, Vénéreau, Emilie, Careccia, G, Saclier, M, Tirone, M, Ruggieri, E, Principi, E, Raffaghello, L, Torchio, S, Recchia, D, Canepari, M, Gorzanelli, A, Ferrara, M, Castellani, P, Rubartelli, A, Rovere-Querini, P, Casalgrandi, M, Preti, A, Lorenzetti, I, Bruno, C, Bottinelli, R, Brunelli, S, Previtali, S, Bianchi, M, Messina, G, Vénéreau, E, Careccia, Giorgia, Saclier, Marielle, Tirone, Mario, Ruggieri, Elena, Principi, Elisa, Raffaghello, Lizzia, Torchio, Silvia, Recchia, Deborah, Canepari, Monica, Gorzanelli, Andrea, Ferrara, Michele, Castellani, Patrizia, Rubartelli, Anna, Rovere-Querini, Patrizia, Casalgrandi, Maura, Preti, Alessandro, Lorenzetti, Isabella, Bruno, Claudio, Bottinelli, Roberto, Brunelli, Silvia, Previtali, Stefano Carlo, Bianchi, Marco Emilio, Messina, Graziella, and Vénéreau, Emilie

Abstract

Muscular dystrophies (MDs) are a group of genetic diseases characterized by progressive muscle wasting associated to oxidative stress and persistent inflammation. It is essential to deepen our knowledge on the mechanism connecting these two processes because current treatments for MDs have limited efficacy and/or are associated with side effects. Here, we identified the alarmin high-mobility group box 1 (HMGB1) as a functional link between oxidative stress and inflammation in MDs. The oxidation of HMGB1 cysteines switches its extracellular activities from the orchestration of tissue regeneration to the exacerbation of inflammation. Extracellular HMGB1 is present at high amount and undergoes oxidation in patients with MDs and in mouse models of Duchenne muscular dystrophy (DMD) and limb-girdle muscular dystrophy 3 (LGMDR3) compared to controls. Genetic ablation of HMGB1 in muscles of DMD mice leads to an amelioration of the dystrophic phenotype as evidenced by the reduced inflammation and muscle degeneration, indicating that HMGB1 oxidation is a detrimental process in MDs. Pharmacological treatment with an engineered nonoxidizable variant of HMGB1, called 3S, improves functional performance, muscle regeneration, and satellite cell engraftment in dystrophic mice while reducing inflammation and fibrosis. Overall, our data demonstrate that the balance between HMGB1 redox isoforms dictates whether skeletal muscle is in an inflamed or regenerating state, and that the nonoxidizable form of HMGB1 is a possible therapeutic approach to counteract the progression of the dystrophic phenotype. Rebalancing the HMGB1 redox isoforms may also be a therapeutic strategy for other disorders characterized by chronic oxidative stress and inflammation.

Published
2021

9. Rebalancing expression of HMGB1 redox isoforms to counteract muscular dystrophy

Author

Careccia, Giorgia, primary, Saclier, Marielle, additional, Tirone, Mario, additional, Ruggieri, Elena, additional, Principi, Elisa, additional, Raffaghello, Lizzia, additional, Torchio, Silvia, additional, Recchia, Deborah, additional, Canepari, Monica, additional, Gorzanelli, Andrea, additional, Ferrara, Michele, additional, Castellani, Patrizia, additional, Rubartelli, Anna, additional, Rovere-Querini, Patrizia, additional, Casalgrandi, Maura, additional, Preti, Alessandro, additional, Lorenzetti, Isabella, additional, Bruno, Claudio, additional, Bottinelli, Roberto, additional, Brunelli, Silvia, additional, Previtali, Stefano Carlo, additional, Bianchi, Marco Emilio, additional, Messina, Graziella, additional, and Vénéreau, Emilie, additional

Published
2021
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10. Heparin protects human neural progenitor cells from Zika Virus-induced cell death and preserves their differentiation into mature neural-glia cells

Author

Pagani, Isabel, primary, Ottoboni, Linda, additional, Podini, Paola, additional, Ghezzi, Silvia, additional, Brambilla, Elena, additional, Bezukladova, Svetlana, additional, Corti, Davide, additional, Bianchi, Marco Emilio, additional, Capobianchi, Maria Rosaria, additional, Yates, Edwin A, additional, Martino, Gianvito, additional, and Vicenzi, Elisa, additional

Published
2021
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14. HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4

Author

Schiraldi, Milena, Raucci, Angela, Martínez Muñoz, Laura, Livoti, Elsa, Celona, Barbara, Venereau, Emilie, Apuzzo, Tiziana, De Marchis, Francesco, Pedotti, Mattia, Bachi, Angela, Thelen, Marcus, Varani, Luca, Mellado, Mario, Proudfoot, Amanda, Bianchi, Marco Emilio, Uguccioni, Mariagrazia, Schiraldi, Milena, Raucci, Angela, Martínez Muñoz, Laura, Livoti, Elsa, Celona, Barbara, Venereau, Emilie, Apuzzo, Tiziana, De Marchis, Francesco, Pedotti, Mattia, Bachi, Angela, Thelen, Marcus, Varani, Luca, Mellado, Mario, Proudfoot, Amanda, Bianchi, Marco Emilio, and Uguccioni, Mariagrazia

Abstract

After tissue damage, inflammatory cells infiltrate the tissue and release proinflammatory cytokines. HMGB1 (high mobility group box 1), a nuclear protein released by necrotic and severely stressed cells, promotes cytokine release via its interaction with the TLR4 (Toll-like receptor 4) receptor and cell migration via an unknown mechanism. We show that HMGB1- induced recruitment of inflammatory cells depends on CXCL12. HMGB1 and CXCL12 form a heterocomplex, which we characterized by nuclear magnetic resonance and surface plasmon resonance, that acts exclusively through CXCR4 and not through other HMGB1 receptors. Fluorescence resonance energy transfer data show that the HMGB1–CXCL12 heterocomplex promotes different conformational rearrangements of CXCR4 from that of CXCL12 alone. Mononuclear cell recruitment in vivo into air pouches and injured muscles depends on the heterocomplex and is inhibited by AMD3100 and glycyrrhizin. Thus, inflammatory cell recruitment and activation both depend on HMGB1 via different mechanisms.

Published
2019

15. High mobility group box 1 orchestrates tissue regeneration via CXCR4

Author

Tirone, M, Tran, N, Ceriotti, C, Gorzanelli, A, Canepari, M, Bottinelli, R, Raucci, A, Di Maggio, S, Santiago, C, Mellado, M, Saclier, M, François, S, Careccia, G, He, M, De Marchis, F, Conti, V, Ben Larbi, S, Cuvellier, S, Casalgrandi, M, Preti, A, Chazaud, B, Al-Abed, Y, Messina, G, Sitia, G, Brunelli, S, Bianchi, M, Vénéreau, E, Tirone, Mario, Tran, Ngoc Lan, Ceriotti, Chiara, Gorzanelli, Andrea, Canepari, Monica, Bottinelli, Roberto, Raucci, Angela, Di Maggio, Stefania, Santiago, César, Mellado, Mario, Saclier, Marielle, François, Stéphanie, Careccia, Giorgia, He, Mingzhu, De Marchis, Francesco, Conti, Valentina, Ben Larbi, Sabrina, Cuvellier, Sylvain, CASALGRANDI, MAURA, Preti, Alessandro, Chazaud, Bénédicte, Al-Abed, Yousef, Messina, Graziella, Sitia, Giovanni, Brunelli, Silvia, Bianchi, Marco Emilio, Vénéreau, Emilie, Tirone, M, Tran, N, Ceriotti, C, Gorzanelli, A, Canepari, M, Bottinelli, R, Raucci, A, Di Maggio, S, Santiago, C, Mellado, M, Saclier, M, François, S, Careccia, G, He, M, De Marchis, F, Conti, V, Ben Larbi, S, Cuvellier, S, Casalgrandi, M, Preti, A, Chazaud, B, Al-Abed, Y, Messina, G, Sitia, G, Brunelli, S, Bianchi, M, Vénéreau, E, Tirone, Mario, Tran, Ngoc Lan, Ceriotti, Chiara, Gorzanelli, Andrea, Canepari, Monica, Bottinelli, Roberto, Raucci, Angela, Di Maggio, Stefania, Santiago, César, Mellado, Mario, Saclier, Marielle, François, Stéphanie, Careccia, Giorgia, He, Mingzhu, De Marchis, Francesco, Conti, Valentina, Ben Larbi, Sabrina, Cuvellier, Sylvain, CASALGRANDI, MAURA, Preti, Alessandro, Chazaud, Bénédicte, Al-Abed, Yousef, Messina, Graziella, Sitia, Giovanni, Brunelli, Silvia, Bianchi, Marco Emilio, and Vénéreau, Emilie

Abstract

Inflammation and tissue regeneration follow tissue damage, but little is known about how these processes are coordinated. High Mobility Group Box 1 (HMGB1) is a nuclear protein that, when released on injury, triggers inflammation. We previously showed that HMGB1 with reduced cysteines is a chemoattractant, whereas a disulfide bond makes it a proinflammatory cytokine. Here we report that fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfide HMGB1 and its receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are not involved. Injection of HMGB1 accelerates tissue repair by acting on resident muscle stem cells, hepatocytes, and infiltrating cells. The nonoxidizable HMGB1 mutant 3S, in which serines replace cysteines, promotes muscle and liver regeneration more efficiently than the wildtype protein and without exacerbating inflammation by selectively interacting with CXCR4. Overall, our results show that the reduced form of HMGB1 coordinates tissue regeneration and suggest that 3S may be used to safely accelerate healing after injury in diverse clinical contexts.

Published
2018

16. DAMPs from death to new life

Author

Vénéreau E, Ceriotti C, BIANCHI , MARCO EMILIO, Vénéreau, E, Ceriotti, C, and Bianchi, MARCO EMILIO

Published
2015

18. MP82-14 SINGLE NUCLEOTIDE POLYMORPHISMS AND RISK OF PROSTATE CANCER: DEVELOPMENT AND VALIDATION OF A NOVEL GENETIC RISK SCORE FOR INDIVIDUALIZED SCREENING AND DIAGNOSTIC PROGRAMMES

Author

Cucchiara, Vito, primary, Mirone, Vincenzo, additional, Lazarevic, Dejan, additional, Cittaro, Davide, additional, Tonon, Giovanni, additional, Zoccolillo, Matteo, additional, Bianchi, Marco Emilio, additional, Gandaglia, Giorgio, additional, Fossati, Nicola, additional, Shariat, Shahrokh F, additional, Montorsi, Francesco, additional, and Briganti, Alberto, additional

Published
2018
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19. MP29-17 ASSOCIATION BETWEEN RS6152 POLYMORPHISM IN THE ANDROGEN RECEPTOR GENE AND DISEASE AGGRESSIVENESS IN A PROSPECTIVE COHORT OF PROSTATE CANCER PATIENTS UNDERGOING RADICAL PROSTATECTOMY

Author

Cucchiara, Vito, primary, Mirone, Vincenzo, additional, Lazarevic, Dejan, additional, Cittaro, Davide, additional, Tonon, Giovanni, additional, Zoccolillo, Matteo, additional, Bianchi, Marco Emilio, additional, Montironi, Rodolfo, additional, Gandaglia, Giorgio, additional, Fossati, Nicola, additional, Shariat, Shahrokh F, additional, Montorsi, Francesco, additional, and Briganti, Alberto, additional

Published
2018
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22. Histone content increases in differentiating Embryonic Stem Cells

Author

Karnavas T, Pintonello L, Agresti A, BIANCHI , MARCO EMILIO, Karnavas, T, Pintonello, L, Agresti, A, and Bianchi, MARCO EMILIO

Subjects
chromatin, histone, embryonic stem cell
Abstract

Mouse Embryonic Stem Cells (ESCs) are pluripotent mammalian cells derived from the Inner Cell Mass (ICM) of mouse blastocysts, which give rise to all three embryonic germ layers both in vivo and in vitro. Mouse ESCs have a distinct epigenetic landscape and a more decondensed chromatin compared to differentiated cells. Numerous studies have shown that distinct histone modifications in ESCs serve as hallmarks of pluripotency. However, so far it is still unknown whether the total histone content (as opposed to histone modifications) remains the same in cells of different developmental stage and differentiation capacity. In this work we show that total histone content differs between pluripotent and differentiated cells. In vitro spontaneous differentiation from ESCs to Embryoid Bodies (EBs) and directed differentiation toward neuronal and endodermal cells entails an increase in histone content. Primary MEFs also contain more histones than ESCs. We suggest that the difference in histone content is an additional hallmark of pluripotency, in addition to and besides histone modifications.

Published
2014

23. Disulfide-containing High Mobility Group Box-1 promotes N-methyl-D-aspartate receptor function and excitotoxicity by activating Toll-Like Receptor 4-dependent signaling in hippocampal neurons

Author

Balosso S, Liu J, BIANCHI , MARCO EMILIO, Vezzani A., Balosso, S, Liu, J, Bianchi, MARCO EMILIO, and Vezzani, A.

Subjects
HMGB1, inflammation, brain
Abstract

Aims: Using primary cultures of mouse hippocampal neurons, we studied the molecular and functional interactionsbetween high mobility group box-1 (HMGB1) and the N-methyl-d-aspartate receptor (NMDAR), twoproteins playing a key role in neuronal hyperexcitability. By measuring NMDA-induced calcium (Ca2+) increasein neuronal somata and neurotoxicity as functional read-out parameters, we explored the role of the redox stateof HMGB1, the receptor involved, and the molecular signaling underlying its interactions with postsynapticNMDAR. We also investigated whether HMGB1 redox state affects its proconvulsive effects in mice. Results:Nonoxidizable HMGB1 with a triple cysteine-to-serine replacement (3S-HMGB1) was ineffective on NMDAresponse. Conversely, the disulfide-containing form of HMGB1 dose dependently enhanced NMDA-inducedCa2+ increase in neuronal cell bodies. This effect was prevented by BoxA, a competitive HMGB1 antagonist, andby Rhodobacter sphaeroides lipopolysaccharide (LPS-RS), a toll-like receptor 4 (TLR4) selective antagonist, andit was abrogated in neurons lacking TLR4 while persisting in the absence of receptor for advanced glycation endproducts (RAGE). TLR4 and NMDAR subunit 1 (NR1) and 2B (NR2B) were colocalized in neurons. DisulfideHMGB1 effect on NMDA-induced Ca2+ influx was prevented by 3-O-methylsphingomyelin (3-O-MS) and 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3,4-d] pyrimidine, (PP2) selective inhibitors of neutral sphingomyelinaseand Src-family Tyr kinases, respectively. Disulfide HMGB1, but not 3S-HMGB1, increased Tyr1472phosphorylation of the NR2B subunit of the NMDAR, which is known to increase Ca2+ channel permeability.Similarly, disulfide HMGB1 increased NMDA-induced neuronal cell death in vitro and enhanced kainate-inducedseizures in vivo. Innovation and Conclusion: We describe a novel molecular neuronal pathway activatedby HMGB1 that could be targeted in vivo to prevent neurodegeneration and seizures mediated by excessiveNMDARs stimulation.

Published
2014

24. A simple model of NF-kappaB dynamics reproduces experimental observations

Author

Zambrano S, BIANCHI , MARCO EMILIO, Agresti A., Zambrano, S, Bianchi, MARCO EMILIO, and Agresti, A.

Abstract

The mathematical modeling of the NF-κB oscillations has attracted considerable attention in recent times, but there is a lack of simple models in the literature that can capture the main features of the dynamics of this important transcription factor. For this reason we propose a simple model that summarizes the key steps of the NF-κB pathway. We show that the resulting 5-dimensional dynamical system can reproduce different phenomena observed in experiments. Our model can display smooth and spiky oscillations in the amount of nuclear NF-κB and can reproduce the variety of dynamics observed when different stimulations such as TNF-α and LPS are used. Furthermore we show that the model can be easily extended to reproduce the expression of early, intermediate and late genes upon stimulation. As a final example we show that our simple model can mimic the different transcriptional outputs observed when cells are treated with two different drugs leading to nuclear localization of NF-κB: Leptomycin B and Cycloheximide.

Published
2014

25. High mobility group box 1 orchestrates tissue regeneration via CXCR4

Author

Tirone, Mario, primary, Tran, Ngoc Lan, additional, Ceriotti, Chiara, additional, Gorzanelli, Andrea, additional, Canepari, Monica, additional, Bottinelli, Roberto, additional, Raucci, Angela, additional, Di Maggio, Stefania, additional, Santiago, César, additional, Mellado, Mario, additional, Saclier, Marielle, additional, François, Stéphanie, additional, Careccia, Giorgia, additional, He, Mingzhu, additional, De Marchis, Francesco, additional, Conti, Valentina, additional, Ben Larbi, Sabrina, additional, Cuvellier, Sylvain, additional, Casalgrandi, Maura, additional, Preti, Alessandro, additional, Chazaud, Bénédicte, additional, Al-Abed, Yousef, additional, Messina, Graziella, additional, Sitia, Giovanni, additional, Brunelli, Silvia, additional, Bianchi, Marco Emilio, additional, and Vénéreau, Emilie, additional

Published
2017
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26. Leukocyte Hmgb1 controls the regeneration and vascularization of acutely damaged skeletal muscle

Author

Campana L, Santarella F, Rigamonti E, Monno A, Canu T, ESPOSITO, ANTONIO, DEL MASCHIO, ALESSANDRO, BIANCHI, MARCO EMILIO, MANFREDI, ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, Campana, L, Santarella, F, Rigamonti, E, Monno, A, Esposito, Antonio, Canu, T, DEL MASCHIO, Alessandro, Bianchi, MARCO EMILIO, Manfredi, ANGELO ANDREA M. A., and ROVERE QUERINI, Patrizia

Published
2013

27. Spatial distribution of positive cores improves the selection of patients with low-risk prostate cancer as candidates for active surveillance

Author

Abdollah, F, Suardi, N, Capitanio, U, Gallina, A, Sun, M, Villa, L, Scattoni, V, BIANCHI, MARCO EMILIO, Tutolo, M, Fossati, N, Karakiewicz, P, RIGATTI, PATRIZIO, MONTORSI, FRANCESCO, BRIGANTI, ALBERTO, Abdollah, F, Suardi, N, Capitanio, U, Gallina, A, Sun, M, Villa, L, Scattoni, V, Bianchi, MARCO EMILIO, Tutolo, M, Fossati, N, Karakiewicz, P, Rigatti, Patrizio, Montorsi, Francesco, and Briganti, Alberto

Subjects
Male, spatial distribution, Risk Factor, Patient Selection, Medicine (all), Urology, active surveillance, positive core, Middle Aged, prostate cancer, Retrospective Studie, Prostatic Neoplasm, prostate biopsy, Watchful Waiting, Human
Abstract

Objective To test the hypothesis that spatial distribution of positive cores at biopsy is a predictor of unfavourable prostate cancer characteristics at radical prostatectomy (RP) in active surveillance (AS) candidates. Patients and Methods We examined the data of 524 patients treated with RP, between 2000 and 2012. All fulfilled at least one of four commonly used AS criteria. Regression models tested the relationship between positive cores spatial distribution, defined as the number of positive zones at biopsy (PBxZ) and tumour laterality at biopsy and two endpoints: (i) unfavourable prostate cancer at RP (Gleason score 4 + 3, and/or pT3 disease), and (ii) clinically significant prostate cancer (tumour volume 2.5mL). Results Unfavourable prostate cancer and clinically significant prostate cancer rates were 8 and 25%, respectively. Patients with more than one PBxZ had a 3.2-fold higher risk of harbouring unfavourable prostate cancer, and a 2.3-fold higher risk of harbouring clinically significant prostate cancer compared with their counterparts with one PBxZ (both P = 0.01). Patients with bilateral tumour at biopsy had a 3.3-fold higher risk of harbouring unfavourable prostate cancer and a 1.7-fold higher risk of harbouring clinically significant prostate cancer compared with their counterparts with unilateral tumour at biopsy (both P 0.04). Some of these results did not reach a statistically significant level, when the analyses were restricted to patients that fulfilled the most stringent AS criteria. Conclusions Positive cores spatial distribution at biopsy should be considered, when advising patients about AS. The addition of this predictor to AS inclusion criteria can help identifying patients at a higher risk of progression, and reduce the rate of inappropriate surveillance of aggressive tumours. However, the most stringent AS criteria (namely John-Hopkins criteria and Prostate Cancer Research International: Active Surveillance criteria) might not benefit from the addition of this predictor. This point warrants further investigation in future studies.

Published
2013

28. Receptor for Advanced Glycation Endproducts is upregulated in temporal lobe epilepsy and contributes to experimental seizures

Author

Iori V, Maroso M, Rizzi M, Iyer AM, Vertemara R, Carli M, Agresti A, Antonelli A, Aronica E, Ravizza T, Vezzani A., BIANCHI , MARCO EMILIO, Iori, V, Maroso, M, Rizzi, M, Iyer, Am, Vertemara, R, Carli, M, Agresti, A, Antonelli, A, Bianchi, MARCO EMILIO, Aronica, E, Ravizza, T, and Vezzani, A.

Abstract

Toll-like receptor 4 (TLR4) activation in neuron and astrocytes by High Mobility Group Box 1 (HMGB1) protein is a key mechanism of seizure generation. HMGB1 also activates the Receptor for Advanced Glycation Endproducts (RAGE), but it was unknown whether RAGE activation contributes to seizures or to HMGB1 proictogenic effects. We found that acute EEG seizures induced by 7ng intrahippocampal kainic acid (KA) were significantly reduced in Rage-/- mice relative to wild type (Wt) mice. The proictogenic effect of HMGB1 was decreased in Rage-/- mice, but less so, than in Tlr4-/- mice. In a mouse mesial temporal lobe epilepsy (mTLE) model, status epilepticus induced by 200ng intrahippocampal KA and the onset of the spontaneous epileptic activity were similar in Rage-/-, Tlr4-/- and Wt mice. However, the number of hippocampal paroxysmal episodes and their duration were both decreased in epileptic Rage-/- and Tlr4-/- mice vs Wt mice. All strains of epileptic mice displayed similar cognitive deficits in the novel object recognition test vs the corresponding control mice. CA1 neuronal cell loss was increased in epileptic Rage-/- vs epileptic Wt mice, while granule cell dispersion and doublecortin (DCX)-positive neurons were similarly affected. Notably, DCX neurons were preserved in epileptic Tlr4-/- mice. We did not find compensatory changes in HMGB1-related inflammatory signaling nor in glutamate receptor subunits in Rage-/- and Tlr4-/- naïve mice, except for ~20% NR2B subunit reduction in Rage-/- mice. RAGE was induced in neurons, astrocytes and microvessels in human and experimental mTLE hippocampi. We conclude that RAGE contributes to hyperexcitability underlying acute and chronic seizures, as well as to the proictogenic effects of HMGB1. RAGE and TLR4 play different roles in the neuropathologic sequelae developing after status epilepticus. These findings reveal new molecular mechanisms underlying seizures, cell loss and neurogenesis which involve inflammatory pathways upregulated in human epilepsy.

Published
2013

30. The effect of annual surgical caseload on the rates of in-hospital pneumonia and other in-hospital outcomes after radical prostatectomy

Author

Schmitges, J., Trinh Q. . , D., BIANCHI, MARCO EMILIO, Sun, M., Abdollah, F., Ahyai S. , A., Jeldres, C., Steuber, T., Perrotte, P., Shariat S. , F., Menon, M., MONTORSI, FRANCESCO, Graefen, M., Karakiewicz P. , I., Schmitges, J., Trinh Q. ., D., Bianchi, MARCO EMILIO, Sun, M., Abdollah, F., Ahyai S., A., Jeldres, C., Steuber, T., Perrotte, P., Shariat S., F., Menon, M., Montorsi, Francesco, Graefen, M., and Karakiewicz P., I.

Published
2012

37. Redox remodeling: a candidate regulator of HMGB1 function in injured skeletal muscle

Author

Vezzoli M, Castellani P, Campana L, Coma G, Bosurgi L, MANFREDI , ANGELO ANDREA M. A., BIANCHI , MARCO EMILIO, Rubartelli A, ROVERE QUERINI , PATRIZIA, Vezzoli, M, Castellani, P, Campana, L, Coma, G, Bosurgi, L, Manfredi, ANGELO ANDREA M. A., Bianchi, MARCO EMILIO, Rubartelli, A, and ROVERE QUERINI, Patrizia

Published
2010

38. Inhibitor of NF-kappa B kinases alpha and beta are both essential for high mobility group box 1-mediated chemotaxis

Author

Penzo M, Molteni R, Suda T, Samaniego S, Raucci A, Habiel DM, Miller F, Jiang HP, Li J, PARDI , RUGGERO, Palumbo R, Olivotto E, Kew RR, BIANCHI, MARCO EMILIO, Marcu K.B., Penzo, M, Molteni, R, Suda, T, Samaniego, S, Raucci, A, Habiel, Dm, Miller, F, Jiang, Hp, Li, J, Pardi, Ruggero, Palumbo, R, Olivotto, E, Kew, Rr, Bianchi, MARCO EMILIO, and Marcu, K. B.

Abstract

Inhibitor of NF-kappaB kinases beta (IKKbeta) and alpha (IKKalpha) activate distinct NF-kappaB signaling modules. The IKKbeta/canonical NF-kappaB pathway rapidly responds to stress-like conditions, whereas the IKKalpha/noncanonical pathway controls adaptive immunity. Moreover, IKKalpha can attenuate IKKbeta-initiated inflammatory responses. High mobility group box 1 (HMGB1), a chromatin protein, is an extracellular signal of tissue damage-attracting cells in inflammation, tissue regeneration, and scar formation. We show that IKKalpha and IKKbeta are each critically important for HMGB1-elicited chemotaxis of fibroblasts, macrophages, and neutrophils in vitro and neutrophils in vivo. By time-lapse microscopy we dissected different parameters of the HMGB1 migration response and found that IKKalpha and IKKbeta are each essential to polarize cells toward HMGB1 and that each kinase also differentially affects cellular velocity in a time-dependent manner. In addition, HMGB1 modestly induces noncanonical IKKalpha-dependent p52 nuclear translocation and p52/RelB target gene expression. Akin to IKKalpha and IKKbeta, p52 and RelB are also required for HMGB1 chemotaxis, and p52 is essential for cellular orientation toward an HMGB1 gradient. RAGE, a ubiquitously expressed HMGB1 receptor, is required for HMGB1 chemotaxis. Moreover, IKKbeta, but not IKKalpha, is required for HMGB1 to induce RAGE mRNA, suggesting that RAGE is at least one IKKbeta target involved in HMGB1 migration responses, and in accord with these results enforced RAGE expression rescues the HMGB1 migration defect of IKKbeta, but not IKKalpha, null cells. Thus, proinflammatory HMGB1 chemotactic responses mechanistically require the differential collaboration of both IKK-dependent NF-kappaB signaling pathways.

Published
2010

39. HMGB1 CONTAINING NUCLEOSOMES FROM APOPTOTIC CELLS INDUCE INFLAMMATION AND IMMUNE ACTIVATION VIA TLR2-IMPLICATIONS FOR THE ETIOPATHOGENESIS OF SYSTEMIC LUPUS ERYTHEMATOSUS RID E-7725-2010

Author

Urbonaviciute, V, Fuernrohr, Bg, Meister, S, Munoz, L, Heyder, P, De Marchis, F, Kirschning, C, Wagner, H, Kalden, Jr, Schett, G, Herrmann, M, Voll, Re, BIANCHI, MARCO EMILIO, MANFREDI, ANGELO ANDREA M. A., ROVERE QUERINI, PATRIZIA, Urbonaviciute, V, Fuernrohr, Bg, Meister, S, Munoz, L, Heyder, P, De Marchis, F, Bianchi, MARCO EMILIO, Kirschning, C, Wagner, H, Manfredi, ANGELO ANDREA M. A., Kalden, Jr, Schett, G, ROVERE QUERINI, Patrizia, Herrmann, M, and Voll, Re

Published
2010

41. HMGB proteins function as universal sentinels for nucleic acid-mediated innate immune responses

Author

Yanai, H, Ban, T, Wang, Zc, Choi, Mk, Kawamura, T, Negishi, H, Nakasato, M, Lu, Y, Hangai, S, Koshiba, R, Savitsky, D, Ronfani, L, Akira, S, Honda, K, Tamura, T, Kodama, T, Taniguchi, T., BIANCHI, MARCO EMILIO, Yanai, H, Ban, T, Wang, Zc, Choi, Mk, Kawamura, T, Negishi, H, Nakasato, M, Lu, Y, Hangai, S, Koshiba, R, Savitsky, D, Ronfani, L, Akira, S, Bianchi, MARCO EMILIO, Honda, K, Tamura, T, Kodama, T, and Taniguchi, T.

Abstract

The activation of innate immune responses by nucleic acids iscrucial to protective and pathological immunities and is mediatedby the transmembrane Toll-like receptors (TLRs) and cytosolicreceptors1,2. However, it remains unknown whether a mechanismexists that integrates these nucleic-acid-sensing systems. Here weshow that high-mobility group box (HMGB) proteins 1, 2 and 3function as universal sentinels for nucleic acids.HMGBs bind to allimmunogenic nucleic acids examined with a correlation betweenaffinity and immunogenic potential. Hmgb12/2 and Hmgb22/2mouse cells are defective in type-I interferon and inflammatorycytokine induction by DNA or RNA targeted to activate the cytosolicnucleic-acid-sensing receptors; cells in which the expressionof all three HMGBs is suppressed show a more profound defect,accompanied by impaired activation of the transcription factorsinterferon regulatory factor 3 (IRF3) and nuclear factor (NF)-kB.The absence of HMGBs also severely impairs the activation ofTLR3, TLR7 and TLR9 by their cognate nucleic acids. Our resultstherefore indicate a hierarchy in the nucleic-acid-mediated activationof immune responses, wherein the selective activation ofnucleic-acid-sensing receptors is contingent on the more promiscuoussensing of nucleic acids byHMGBs. These findings may haveimplications for understanding the evolution of the innate immunesystem and for the treatment of immunological disorders.

Published
2009

42. HMGB1 loves company

Author

BIANCHI , MARCO EMILIO and Bianchi, MARCO EMILIO

Published
2009

43. HMGB1-Nucleosome complexes from apoptotic cells initiate proinflammatory responses and induce Anti-DsDNA antibodies in mice

Author

Urbonaviciute, V, Furnrohr, Bg, Meister, S, Munoz, L, Heyder, P, Kalden, J, Herrmann, M, Voll, Re, MANFREDI, ANGELO ANDREA M. A., BIANCHI, MARCO EMILIO, ROVERE QUERINI, PATRIZIA, Urbonaviciute, V, Furnrohr, Bg, Meister, S, Munoz, L, Heyder, P, Kalden, J, Manfredi, ANGELO ANDREA M. A., Bianchi, MARCO EMILIO, ROVERE QUERINI, Patrizia, Herrmann, M, and Voll, Re

Published
2008

44. The stage-specific secretion of HMGB1 in cartilage regulates endochondral ossification

Author

TANIGUCHI N, YOSHIDA K, ITO T, TSUDA M, MISHIMA Y, FURUMATSU T, RONFANI L, ABEYAMA K, KAWAHARA K, KOMIYA S, MARUYAMA I, LOTZ M, ASAHARA H., BIANCHI , MARCO EMILIO, Taniguchi, N, Yoshida, K, Ito, T, Tsuda, M, Mishima, Y, Furumatsu, T, Ronfani, L, Abeyama, K, Kawahara, K, Komiya, S, Maruyama, I, Lotz, M, Bianchi, MARCO EMILIO, and Asahara, H.

Published
2007

45. HMGB1: a signal of necrosis

Author

RAUCCI A, PALUMBO R, BIANCHI , MARCO EMILIO, Raucci, A, Palumbo, R, and Bianchi, MARCO EMILIO

Published
2007

46. DAMPs, PAMPs and alarmins: all we need to know about danger

Author

BIANCHI , MARCO EMILIO and Bianchi, MARCO EMILIO

Abstract

Multicellular animals detect pathogens via a set of receptors that recognize pathogen associated molecular patterns (PAMPs). However, pathogens are not the only causative agents of tissue and cell damage: trauma is another one. Evidence is accumulating that trauma and its associated tissue damage are recognized at the cell level via receptor-mediated detection of intracellular proteins released by the dead cells. The term “alarmin” is proposed to categorize such endogenous molecules that signal tissue and cell damage. Intriguingly, effector cells of innate and adaptive immunity can secrete alarmins via nonclassical pathways and often do so when they are activated by PAMPs or other alarmins. Endogenous alarmins and exogenous PAMPs therefore convey a similar message and elicit similar responses; they can be considered subgroups of a larger set, the damage associated molecular patterns (DAMPs).

Published
2007

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