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34 results on '"Greene, Lloyd A."'

1. Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance.

Author

Banerjee, Debarshi, Bobolla, Shuobo, Okochi, Shunpei, Kadenhe-Chiweshe, Angela, Lopez, Gonzalo, Califano, Andrea, Connolly, Eileen, Greene, Lloyd, Yamashiro, Darrell, and Angelastro, James

Abstract

UNLABELLED: MYCN-amplified neuroblastoma often presents as a highly aggressive metastatic disease with a poor prognosis. Activating transcription factor 5 (ATF5) is implicated in neural cell differentiation and cancer cell survival. Here, we show that ATF5 is highly expressed in patients with stage 4 high-risk neuroblastoma, with increased expression correlating with a poorer prognosis. We demonstrated that ATF5 promotes the metastasis of neuroblastoma cell lines in vivo. Functionally, ATF5 depletion significantly reduced xenograft tumor growth and metastasis of neuroblastoma cells to the bone marrow and liver. Mechanistically, ATF5 endows tumor cells with resistance to anoikis, thereby increasing their survival in systemic circulation and facilitating metastasis. We identified the proapoptotic BCL-2 modifying factor (BMF) as a critical player in ATF5-regulated neuroblastoma anoikis. ATF5 suppresses BMF under suspension conditions at the transcriptional level, promoting anoikis resistance, whereas BMF knockdown significantly prevents ATF5 depletion-induced anoikis. Therapeutically, we showed that a cell-penetrating dominant-negative ATF5 peptide, CP-d/n-ATF5, inhibits neuroblastoma metastasis to the bone marrow and liver by inducing anoikis sensitivity in circulating tumor cells. Our study identified ATF5 as a metastasis promoter and CP-d/n-ATF5 as a potential antimetastatic therapeutic agent for neuroblastoma. SIGNIFICANCE: This study shows that resistance to anoikis in neuroblastoma is mediated by ATF5 and offers a rationale for targeting ATF5 to treat metastatic neuroblastoma.

Published
2023

2. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, 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 JM, Bianchi, Marco E, Blagosklonny, Mikhail V, Blander, J Magarian, Blandino, Giovanni, Blomgren, Klas, Borner, Christoph, Bortner, Carl D, Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, Thomas, 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, Bart, 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 Maria, Galassi, Claudia, Ganini, Carlo, Garcia-Saez, 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, and Kanneganti, Thirumala-Devi

Subjects
Biochemistry and Cell Biology, Biological Sciences, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic health relevance, Good Health and Well Being, Animals, Humans, Apoptosis, Cell Death, Caspases, Carcinogenesis, Mammals, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
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

4. Targeting Transcription Factors ATF5, CEBPB and CEBPD with Cell-Penetrating Peptides to Treat Brain and Other Cancers

Author

Greene, Lloyd A, Zhou, Qing, Siegelin, Markus D, and Angelastro, James M

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Brain Disorders, Orphan Drug, Genetics, Cancer, Brain Cancer, Neurosciences, Rare Diseases, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Humans, Cell-Penetrating Peptides, Neoplasms, Brain, Drug Development, CCAAT-Enhancer-Binding Protein-delta, Activating Transcription Factors, CCAAT-Enhancer-Binding Protein-beta, brain cancer, glioblastoma, transcription factor, ATF5, CEBPB, CEBPD, dominant-negative, decoy, cell-penetrating, drug, Biological sciences, Biomedical and clinical sciences
Abstract

Developing novel therapeutics often follows three steps: target identification, design of strategies to suppress target activity and drug development to implement the strategies. In this review, we recount the evidence identifying the basic leucine zipper transcription factors ATF5, CEBPB, and CEBPD as targets for brain and other malignancies. We describe strategies that exploit the structures of the three factors to create inhibitory dominant-negative (DN) mutant forms that selectively suppress growth and survival of cancer cells. We then discuss and compare four peptides (CP-DN-ATF5, Dpep, Bpep and ST101) in which DN sequences are joined with cell-penetrating domains to create drugs that pass through tissue barriers and into cells. The peptide drugs show both efficacy and safety in suppressing growth and in the survival of brain and other cancers in vivo, and ST101 is currently in clinical trials for solid tumors, including GBM. We further consider known mechanisms by which the peptides act and how these have been exploited in rationally designed combination therapies. We additionally discuss lacunae in our knowledge about the peptides that merit further research. Finally, we suggest both short- and long-term directions for creating new generations of drugs targeting ATF5, CEBPB, CEBPD, and other transcription factors for treating brain and other malignancies.

Published
2023

5. Second-year results from CINEMA: A novel, patient-centered, team-based intervention for patients with Type 2 diabetes or prediabetes at high cardiovascular risk

Author

Neeland, Ian J., Arafah, Ala’, Bourges-Sevenier, Brendan, Dazard, Jean-Eudes, Albar, Zainab, Landskroner, Zoe, Tashtish, Nour, Eaton, Elke, Friswold, Janice, Porges, Jodie, Nennstiel, Matthew, Davies, Amanda, Rahmani, Sara, Howard, Quiana S., Forrest, Katherine, Sullivan, Claire, Greene, Lloyd, Al-Kindi, Sadeer G., and Rajagopalan, Sanjay

Published
2024
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7. DPEP Inhibits Cancer Cell Glucose Uptake, Glycolysis and Survival by Upregulating Tumor Suppressor TXNIP.

Author

Zhou, Qing, Nguyen, Trang Thi Thu, Mun, Jeong-Yeon, Siegelin, Markus D., and Greene, Lloyd A.

Subjects
GLYCOLYSIS, CANCER cells, METFORMIN, CELL-penetrating peptides, THIOREDOXIN-interacting protein, GLUCOSE, TUMOR suppressor proteins
Abstract

We have designed cell-penetrating peptides that target the leucine zipper transcription factors ATF5, CEBPB and CEBPD and that promote apoptotic death of a wide range of cancer cell types, but not normal cells, in vitro and in vivo. Though such peptides have the potential for clinical application, their mechanisms of action are not fully understood. Here, we show that one such peptide, Dpep, compromises glucose uptake and glycolysis in a cell context-dependent manner (in about two-thirds of cancer lines assessed). These actions are dependent on induction of tumor suppressor TXNIP (thioredoxin-interacting protein) mRNA and protein. Knockdown studies show that TXNIP significantly contributes to apoptotic death in those cancer cells in which it is induced by Dpep. The metabolic actions of Dpep on glycolysis led us to explore combinations of Dpep with clinically approved drugs metformin and atovaquone that inhibit oxidative phosphorylation and that are in trials for cancer treatment. Dpep showed additive to synergistic activities in all lines tested. In summary, we find that Dpep induces TXNIP in a cell context-dependent manner that in turn suppresses glucose uptake and glycolysis and contributes to apoptotic death of a range of cancer cells. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Revolutionizing Brain Tumor Care: Emerging Technologies and Strategies.

Author

Nguyen, Trang T. T., Greene, Lloyd A., Mnatsakanyan, Hayk, and Badr, Christian E.

Subjects
TECHNOLOGICAL innovations, BRAIN tumors, GLIOBLASTOMA multiforme, TUMOR treatment, BLOOD-brain barrier
Abstract

Glioblastoma multiforme (GBM) is one of the most aggressive forms of brain tumor, characterized by a daunting prognosis with a life expectancy hovering around 12–16 months. Despite a century of relentless research, only a select few drugs have received approval for brain tumor treatment, largely due to the formidable barrier posed by the blood–brain barrier. The current standard of care involves a multifaceted approach combining surgery, irradiation, and chemotherapy. However, recurrence often occurs within months despite these interventions. The formidable challenges of drug delivery to the brain and overcoming therapeutic resistance have become focal points in the treatment of brain tumors and are deemed essential to overcoming tumor recurrence. In recent years, a promising wave of advanced treatments has emerged, offering a glimpse of hope to overcome the limitations of existing therapies. This review aims to highlight cutting-edge technologies in the current and ongoing stages of development, providing patients with valuable insights to guide their choices in brain tumor treatment. [ABSTRACT FROM AUTHOR]

Published
2024
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25. Second-Year Results from CINEMA: A Novel, Patient-Centered, Team-Based Intervention for Patients with Type 2 Diabetes or Prediabetes at High Cardiovascular Risk

Author

Neeland, Ian J., primary, Arafah, Ala’, additional, Bourges-Sevenier, Brendan, additional, Dazard, Jean-Eudes, additional, Albar, Zainab, additional, Landskroner, Zoe, additional, Tashtish, Nour, additional, Eaton, Elke, additional, Friswold, Janice, additional, Porges, Jodie, additional, Nennstiel, Matthew, additional, Davies, Amanda, additional, Rahmani, Sara, additional, Howard, Quiana S., additional, Forrest, Katherine, additional, Sullivan, Claire, additional, Greene, Lloyd, additional, Al-Kindi, Sadeer G., additional, and Rajagopalan, Sanjay, additional

Published
2023
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30. 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. 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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

31. Supplementary materials and methods untracked from A Synthetic Cell-Penetrating Dominant-Negative ATF5 Peptide Exerts Anticancer Activity against a Broad Spectrum of Treatment-Resistant Cancers

Author

Karpel-Massler, Georg, primary, Horst, Basil A., primary, Shu, Chang, primary, Chau, Lily, primary, Tsujiuchi, Takashi, primary, Bruce, Jeffrey N., primary, Canoll, Peter, primary, Greene, Lloyd A., primary, Angelastro, James M., primary, and Siegelin, Markus D., primary

Published
2023
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32. Supplementary figure legend unmarked from A Synthetic Cell-Penetrating Dominant-Negative ATF5 Peptide Exerts Anticancer Activity against a Broad Spectrum of Treatment-Resistant Cancers

Author

Karpel-Massler, Georg, primary, Horst, Basil A., primary, Shu, Chang, primary, Chau, Lily, primary, Tsujiuchi, Takashi, primary, Bruce, Jeffrey N., primary, Canoll, Peter, primary, Greene, Lloyd A., primary, Angelastro, James M., primary, and Siegelin, Markus D., primary

Published
2023
Full Text
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33. Supplementary figures 1-15 from A Synthetic Cell-Penetrating Dominant-Negative ATF5 Peptide Exerts Anticancer Activity against a Broad Spectrum of Treatment-Resistant Cancers

Author

Karpel-Massler, Georg, primary, Horst, Basil A., primary, Shu, Chang, primary, Chau, Lily, primary, Tsujiuchi, Takashi, primary, Bruce, Jeffrey N., primary, Canoll, Peter, primary, Greene, Lloyd A., primary, Angelastro, James M., primary, and Siegelin, Markus D., primary

Published
2023
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34. Specific down-regulation of hippocampal ATF4 reveals a necessary role in synaptic plasticity and memory

Author

Pasini, Silvia, Corona, Carlo, Liu, Jin, Greene, Lloyd A., and Shelanski, Michael L.

Abstract

Prior studies suggest that the transcription factor ATF4 negatively regulates synaptic plastic and memory. By contrast, we provide evidence from direct in vitroand in vivoknockdown of ATF4 in rodent hippocampal neurons and from ATF4 null mice that implicate ATF4 as essential for normal synaptic plasticity and memory. In particular, hippocampal ATF4 down-regulation produces deficits in long-term spatial memory and behavioral flexibility without affecting associative memory or anxiety-like behavior. ATF4 knockdown or loss also causes profound impairment of both longterm potentiation (LTP) and long-term depression (LTD) as well as decreased glutamatergic function. We conclude that ATF4 is a key regulator of the physiological state necessary for neuronal plasticity and memory.

Published
2024
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