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558 results on '"Tsujimoto, Yoshihide"'

10. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, Stuart A., Abrams, John M., Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V., Arama, Eli, Baehrecke, Eric H., Barlev, Nickolai A., Bazan, Nicolas G., Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Katiuscia, Blagosklonny, Mikhail V., Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K.-M., Chandel, Navdeep S., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Cohen, Gerald M., Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Dawson, Ted M., Dawson, Valina L., De Laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M., Dixon, Scott J., Duckett, Colin S., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Fimia, Gian Maria, Fulda, Simone, García-Sáez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. Marie, Harris, Isaac S., Hengartner, Michael O., Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, Philipp J., Juin, Philippe P., Kaiser, William J., Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Knight, Richard A., Kumar, Sharad, Lee, Sam W., Lemasters, John J., Levine, Beth, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Lowe, Scott W., Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, Edward A., Molkentin, Jeffery D., Moll, Ute M., Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Piacentini, Mauro, Pinton, Paolo, Prehn, Jochen H.M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rehm, Markus, Rizzuto, Rosario, Rodrigues, Cecilia M.P., Rubinsztein, David C., Rudel, Thomas, Ryan, Kevin M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, Brent R., Strasser, Andreas, Szabadkai, Gyorgy, Tait, Stephen W.G., Tang, Daolin, Tavernarakis, Nektarios, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Boris, Vanden Berghe, Tom, Vandenabeele, Peter, Vander Heiden, Matthew G., Villunger, Andreas, Virgin, Herbert W., Vousden, Karen H., Vucic, Domagoj, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, James A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Boris, Zitvogel, Laurence, Melino, Gerry, and Kroemer, Guido

Published
2018
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38. Bis deficiency results in early lethality with metabolic deterioration and involution of spleen and thymus

Author

Youn, Dong-Ye, Lee, Dong-Hyoung, Lim, Mi-Hyun, Yoon, Jung-Sook, Lim, Ji Hee, Jung, Seung Eun, Yeum, Chung Eun, Park, Cheol Whee, Youn, Ho-Joong, Lee, Jae-Seon, Lee, Seong-Beom, Ikawa, Masahito, Okabe, Masaru, Tsujimoto, Yoshihide, and Lee, Jeong-Hwa

Subjects
Genes -- Physiological aspects, Genes -- Research, Hypoglycemia -- Research, Infants -- Growth, Company growth, Biological sciences
Abstract

Bcl-2 interacting cell death suppressor (Bis), also known as Bag3 or CAIR-1, is involved in antistress and antiapoptotic pathways. In addition to Bcl-2, Bis binds to several proteins, suggesting it has diverse functions in normal and pathological conditions. To better define the physiological function of Bis in vivo, we developed his-deficient mice with a cre-loxP system. Targeted disruption of exon 4 of the bis gene was demonstrated by Southern blotting and PCR, and Western blotting showed that no intact or truncated Bis protein was synthesized in [bis.sup.-/-] mice. While heterozygotes were fertile and appeared normal, Bis-deficient mice showed growth retardation and died by 3 wk after birth. The relative weight of the thymus and spleen was reduced and the total numbers of white blood cells, splenocytes, and thymocytes were significantly reduced compared with wild-type littermates. Serum profiles indicated significant hypoglycemia as well as decrease in triglyceride and cholesterol levels. Expression profiles of metabolic genes indicated that gluconeogenesis and [beta]-oxidation are activated in the liver of [bis.sup.-/-] mice. This activation, as well as a decrease in peripheral fat and an induction of fatty liver, appears to be an adaptive response to hypoglycemia. Our study reveals that the absence of Bis has considerable influences on postnatal growth and survival, possibly due to a nutritional impairment. bis; knockout; hypoglycemia

Published
2008

44. Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death

Author

Nakagawa, Takashi, Shimizu, Shigeomi, Watanabe, Tetsuya, Yamaguchi, Osamu, Otsu, Kinya, Yamagata, Hirotaka, Inohara, Hidenori, Kubo, Takeshi, and Tsujimoto, Yoshihide

Abstract

Author(s): Takashi Nakagawa [1, 2, 4]; Shigeomi Shimizu [1, 4]; Tetsuya Watanabe [3]; Osamu Yamaguchi [3]; Kinya Otsu [3]; Hirotaka Yamagata [1]; Hidenori Inohara [2]; Takeshi Kubo [2]; Yoshihide Tsujimoto [...]

Published
2005
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49. PL[A.sub.2] activity is required for nuclear shrinkage in caspase-independent cell death

Author

Shinzawa, Koei and Tsujimoto, Yoshihide

Subjects
Apoptosis -- Physiological aspects, Cell death -- Physiological aspects, Cell nuclei -- Physiological aspects, Phospholipases -- Physiological aspects, Biological sciences
Abstract

Apoptosis is defined on the basis of morphological changes like nuclear fragmentation and chromatin condensation, which are dependent on caspases. Many forms of caspase-independent cell death have been reported, but the mechanisms are still poorly understood. We found that hypoxic cell death was independent of caspases and was associated with significant nuclear shrinkage. Neither Bcl-2 nor Apaf-1 deficiency prevented hypoxic nuclear shrinkage. To understand the molecular mechanism of the nuclear shrinkage, we developed an in vitro system using permeabilized cells, which allowed us to purify a novel member of the phospholipase [A.sub.2] (PL[A.sub.2]) family that induced nuclear shrinkage. Purified PL[A.sub.2] induced nuclear shrinkage in our permeabilized cell system. PL[A.sub.2] inhibitors prevented hypoxic nuclear shrinkage in cells and cell death. Hypoxia caused elevation of PL[A.sub.2] activity and translocation of intracellular PL[A.sub.2]s to the nucleus. Knockdown of the [Ca.sup.2+]-independent PL[A.sub.2] delayed nuclear shrinkage and cell death. These results indicate that [Ca.sup.2+] -independent PL[A.sub.2] is crucial for a caspase-independent cell death signaling pathway leading to nuclear shrinkage.

Published
2003

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