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348 results on '"Frezza C"'

1. Mitochondrial complex I activity in microglia sustains neuroinflammation

Author

Peruzzotti-Jametti, L., Willis, C. M., Krzak, G., Hamel, R., Pirvan, L., Ionescu, R.-B., Reisz, J. A., Prag, H. A., Garcia-Segura, M. E., Wu, V., Xiang, Y., Barlas, B., Casey, A. M., van den Bosch, A. M. R., Nicaise, A. M., Roth, L., Bates, G. R., Huang, H., Prasad, P., Vincent, A. E., Frezza, C., Viscomi, C., Balmus, G., Takats, Z., Marioni, J. C., D’Alessandro, A., Murphy, M. P., Mohorianu, I., and Pluchino, S.

Published
2024
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2. Mitochondrial reverse electron transport in myeloid cells perpetuates neuroinflammation

Author

Peruzzotti-Jametti, L., primary, Willis, C.M., additional, Hamel, R., additional, Krzak, G., additional, Reisz, J.A., additional, Prag, H.A., additional, Wu, V., additional, Xiang, Y., additional, van den Bosch, A.M.R., additional, Nicaise, A.M., additional, Roth, L., additional, Bates, G.R., additional, Huang, H., additional, Vincent, A.E., additional, Frezza, C., additional, Viscomi, C., additional, Marioni, J.C., additional, D’Alessandro, A., additional, Takats, Z., additional, Murphy, M.P., additional, and Pluchino, S., additional

Published
2024
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4. Fumarate induces vesicular release of mtDNA to drive innate immunity

Author

Zecchini, V., Paupe, V., Herranz-Montoya, I., Janssen, J, Wortel, I.M.N., Morris, J.L., Ferguson, A., Chowdury, S.R., Segarra-Mondejar, M., Costa, A.S.H., Pereira, G.C., Tronci, L., Young, T., Nikitopoulou, E., Yang, M., Bihary, D., Caicci, F., Nagashima, S., Speed, A., Bokea, K., Baig, Z., Samarajiwa, S., Tran, M., Mitchell, T., Johnson, M., Prudent, J., Frezza, C., Zecchini, V., Paupe, V., Herranz-Montoya, I., Janssen, J, Wortel, I.M.N., Morris, J.L., Ferguson, A., Chowdury, S.R., Segarra-Mondejar, M., Costa, A.S.H., Pereira, G.C., Tronci, L., Young, T., Nikitopoulou, E., Yang, M., Bihary, D., Caicci, F., Nagashima, S., Speed, A., Bokea, K., Baig, Z., Samarajiwa, S., Tran, M., Mitchell, T., Johnson, M., Prudent, J., and Frezza, C.

Abstract

Contains fulltext : 290645.pdf (Publisher’s version ) (Open Access)

Published
2023

5. Primary cilia sense glutamine availability and respond via asparagine synthetase.

Author

Steidl, M.E., Nigro, E.A., Nielsen, A.K.S., Pagliarini, R., Cassina, L., Lampis, M., Podrini, C., Chiaravalli, M., Mannella, V., Distefano, G., Yang, M., Aslanyan, M.G., Musco, G., Roepman, R., Frezza, C., Boletta, A., Steidl, M.E., Nigro, E.A., Nielsen, A.K.S., Pagliarini, R., Cassina, L., Lampis, M., Podrini, C., Chiaravalli, M., Mannella, V., Distefano, G., Yang, M., Aslanyan, M.G., Musco, G., Roepman, R., Frezza, C., and Boletta, A.

Abstract

Item does not contain fulltext, Depriving cells of nutrients triggers an energetic crisis, which is resolved by metabolic rewiring and organelle reorganization. Primary cilia are microtubule-based organelles at the cell surface, capable of integrating multiple metabolic and signalling cues, but their precise sensory function is not fully understood. Here we show that primary cilia respond to nutrient availability and adjust their length via glutamine-mediated anaplerosis facilitated by asparagine synthetase (ASNS). Nutrient deprivation causes cilia elongation, mediated by reduced mitochondrial function, ATP availability and AMPK activation independently of mTORC1. Of note, glutamine removal and replenishment is necessary and sufficient to induce ciliary elongation or retraction, respectively, under nutrient stress conditions both in vivo and in vitro by restoring mitochondrial anaplerosis via ASNS-dependent glutamate generation. Ift88-mutant cells lacking cilia show reduced glutamine-dependent mitochondrial anaplerosis during metabolic stress, due to reduced expression and activity of ASNS at the base of cilia. Our data indicate a role for cilia in responding to, and possibly sensing, cellular glutamine levels via ASNS during metabolic stress.

Published
2023

9. Early neutrophilia marked by aerobic glycolysis sustains host 3 metabolism and delays cancer cachexia

Author

Petruzzelli, M, Ferrer, M, Schuijs, MJ, Kleeman, SO, Mourikis, N, Hall, Z, Perera, D, Raghunathan, S, Vacca, M, Gaude, E, Lukey, MJ, Jodrell, DI, Frezza, C, Wagner, EF, Venkitaraman, AR, Halim, TYF, and Janowitz, T

Subjects
host, neutrophils, cancer, 1112 Oncology and Carcinogenesis, aerobic glycolysis, cachexia, metabolism
Abstract

An elevated neutrophil–lymphocyte ratio negatively predicts the outcome of patients with cancer and is associated with cachexia, the terminal wasting syndrome. Here, using murine model systems of colorectal and pancreatic cancer we show that neutrophilia in the circulation and multiple organs, accompanied by extramedullary hematopoiesis, is an early event during cancer progression. Transcriptomic and metabolic assessment reveals that neutrophils in tumor-bearing animals utilize aerobic glycolysis, similar to cancer cells. Although pharmacological inhibition of aerobic glycolysis slows down tumor growth in C26 tumor-bearing mice, it precipitates cachexia, thereby shortening the overall survival. This negative effect may be explained by our observation that acute depletion of neutrophils in pre-cachectic mice impairs systemic glucose homeostasis secondary to altered hepatic lipid processing. Thus, changes in neutrophil number, distribution, and metabolism play an adaptive role in host metabolic homeostasis during cancer progression. Our findings provide insight into early events during cancer progression to cachexia, with implications for therapy.

Published
2022

10. Succinate is an inflammatory signal that induces IL-1β through HIF-1α

Author

Tannahill, G.M., Curtis, A.M., Adamik, J., Palsson-McDermott, E.M., McGettrick, A.F., Goel, G., Frezza, C., Bernard, N.J., Kelly, B., Foley, N.H., Zheng, L., Gardet, A., Tong, Z., Jany, S.S., Corr, S.C., Haneklaus, M., Caffrey, B., Pierce, K., Walmsley, S., Beasley, F.C., Cummins, E., Nizet, V., Whyte, M., Taylor, C.T., Lin, H., Masters, S.L., Gottlieb, E., Kelly, V.P., Clish, C., Auron, P.E., Xavier, R.J., and O'Neill, L.A.J.

Subjects
Inflammation -- Physiological aspects, Macrophages -- Physiological aspects, Interleukins -- Health aspects, Succinates -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Macrophages activated by the Gram-negative bacterial product lipopolysaccharide switch their core metabolism from oxidative phosphorylation to glycolysis (1). Here we show that inhibition of glycolysis with 2-deoxyglucose suppresses lipopolysaccharide-induced interleukin-1β [...]

Published
2013

11. Causal integration of multi-omics data with prior knowledge to generate mechanistic hypotheses

Author

Dugourd, A. (Aurelien), Kuppe, C. (Christoph), Sciacovelli, M. (Marco), Gjerga, E. (Enio), Gabor, A. (Attila), Emdal, K.B. (Kristina B.), Vieira, V. (Vitor), Bekker-Jensen, D.B. (Dorte B.), Kranz, J. (Jennifer), Bindels, E.M.J. (Eric), Costa, A.S.H. (Ana S.H.), Sousa, A. (Abel), Beltrao, P. (Pedro), Rocha, M. (Miguel), Olsen, J.V. (Jesper V.), Frezza, C. (Christian), Kramann, R.J.T. (Rafael), Saez-Rodriguez, J. (Julio), Dugourd, A. (Aurelien), Kuppe, C. (Christoph), Sciacovelli, M. (Marco), Gjerga, E. (Enio), Gabor, A. (Attila), Emdal, K.B. (Kristina B.), Vieira, V. (Vitor), Bekker-Jensen, D.B. (Dorte B.), Kranz, J. (Jennifer), Bindels, E.M.J. (Eric), Costa, A.S.H. (Ana S.H.), Sousa, A. (Abel), Beltrao, P. (Pedro), Rocha, M. (Miguel), Olsen, J.V. (Jesper V.), Frezza, C. (Christian), Kramann, R.J.T. (Rafael), and Saez-Rodriguez, J. (Julio)

Abstract

Multi-omics datasets can provide molecular insights beyond the sum of individual omics. Various tools have been recently developed to integrate such datasets, but there are limited strategies to systematically extract mechanistic hypotheses from them. Here, we present COSMOS (Causal Oriented Search of Multi-Omics Space), a method that integrates phosphoproteomics, transcriptomics, and metabolomics datasets. COSMOS combines extensive prior knowledge of signaling, metabolic, and gene regulatory networks with computational methods to estimate activities of transcription factors and kinases as well as network-level causal reasoning. COSMOS provides mechanistic hypotheses for experimental observations across multi-omics datasets. We applied COSMOS to a dataset comprising transcriptomics, phosphoproteomics, and metabolomics data from healthy and cancerous tissue from eleven clear cell renal cell carcinoma (ccRCC) patients. COSMOS was able to capture relevant crosstalks within and between multiple omics layers, such as known ccRCC drug targets. We expect that our freely available method will be broadly useful to extract mechanistic insights from multi-omics studies.

Published
2021
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12. Causal integration of multi-omics data with prior knowledge to generate mechanistic hypotheses

Author

Dugourd, A, Kuppe, C, Sciacovelli, M, Gjerga, E, Gabor, A, Emdal, KB, Vieira, V, Bekker-Jensen, DB, Kranz, J, Bindels, Eric, Costa, ASH, Sousa, A, Beltrao, P, Rocha, M, Olsen, JV, Frezza, C, Kramann, Rafael, Saez-Rodriguez, J, Dugourd, A, Kuppe, C, Sciacovelli, M, Gjerga, E, Gabor, A, Emdal, KB, Vieira, V, Bekker-Jensen, DB, Kranz, J, Bindels, Eric, Costa, ASH, Sousa, A, Beltrao, P, Rocha, M, Olsen, JV, Frezza, C, Kramann, Rafael, and Saez-Rodriguez, J

Abstract

Multi-omics datasets can provide molecular insights beyond the sum of individual omics. Various tools have been recently developed to integrate such datasets, but there are limited strategies to systematically extract mechanistic hypotheses from them. Here, we present COSMOS (Causal Oriented Search of Multi-Omics Space), a method that integrates phosphoproteomics, transcriptomics, and metabolomics datasets. COSMOS combines extensive prior knowledge of signaling, metabolic, and gene regulatory networks with computational methods to estimate activities of transcription factors and kinases as well as network-level causal reasoning. COSMOS provides mechanistic hypotheses for experimental observations across multi-omics datasets. We applied COSMOS to a dataset comprising transcriptomics, phosphoproteomics, and metabolomics data from healthy and cancerous tissue from eleven clear cell renal cell carcinoma (ccRCC) patients. COSMOS was able to capture relevant crosstalks within and between multiple omics layers, such as known ccRCC drug targets. We expect that our freely available method will be broadly useful to extract mechanistic insights from multi-omics studies.

Published
2021

16. Protection against cardiac ischemia-reperfusion injury by hypothermia and by inhibition of succinate accumulation and oxidation is additive

Author

Kohlhauer, M, Pell, VR, Burger, N, Spiroski, AM, Gruszczyk, A, Mulvey, JF, Mottahedin, Amin, Costa, ASH, Frezza, C, Ghaleh, B, Murphy, MP, Tissier, R, Krieg, T, Krieg, T [0000-0002-5192-580X], and Apollo - University of Cambridge Repository

Subjects
Male, Succinate, Succinic Acid, Myocardial Reperfusion Injury, Hypothermia, Malonates, Myocardial infarction, Random Allocation, Ischemia, Hypothermia, Induced, Reperfusion, Animals, cardiovascular diseases, Rabbits, Dimethyl malonate
Abstract

Hypothermia induced at the onset of ischemia is a potent experimental cardioprotective strategy for myocardial infarction. The aim of our study was to determine whether the beneficial effects of hypothermia may be due to decreasing mitochondria-mediated mechanisms of damage that contribute to the pathophysiology of ischemia/reperfusion injury. New Zealand male rabbits were submitted to 30 min of myocardial ischemia with hypothermia (32 °C) induced by total liquid ventilation (TLV). Hypothermia was applied during ischemia alone (TLV group), during ischemia and reperfusion (TLV-IR group) and normothermia (Control group). In all the cases, ischemia was performed by surgical ligation of the left anterior descending coronary artery and was followed by 3 h of reperfusion before assessment of infarct size. In a parallel study, male C57BL6/J mice underwent 30 min myocardial ischemia followed by reperfusion under either normothermia (37 °C) or conventionally induced hypothermia (32 °C). In both the models, the levels of the citric acid cycle intermediate succinate, mitochondrial complex I activity were assessed at various times. The benefit of hypothermia during ischemia on infarct size was compared to inhibition of succinate accumulation and oxidation by the complex II inhibitor malonate, applied as the pro-drug dimethyl malonate under either normothermic or hypothermic conditions. Hypothermia during ischemia was cardioprotective, even when followed by normothermic reperfusion. Hypothermia during ischemia only, or during both, ischemia and reperfusion, significantly reduced infarct size (2.8 ± 0.6%, 24.2 ± 3.0% and 49.6 ± 2.6% of the area at risk, for TLV-IR, TLV and Control groups, respectively). The significant reduction of infarct size by hypothermia was neither associated with a decrease in ischemic myocardial succinate accumulation, nor with a change in its rate of oxidation at reperfusion. Similarly, dimethyl malonate infusion and hypothermia during ischemia additively reduced infarct size (4.8 ± 2.2% of risk zone) as compared to either strategy alone. Hypothermic cardioprotection is neither dependent on the inhibition of succinate accumulation during ischemia, nor of its rapid oxidation at reperfusion. The additive effect of hypothermia and dimethyl malonate on infarct size shows that they are protective by distinct mechanisms and also suggests that combining these different therapeutic approaches could further protect against ischemia/reperfusion injury during acute myocardial infarction.

Published
2019
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17. Metabolomic profiling in acute ST‐segment–elevation myocardial infarction identifies succinate as an early marker of human ischemia–reperfusion injury

Author

Kohlhauer, M, Dawkins, S, Costa, A, Lee, R, Young, T, Pell, V, Choudhury, R, Banning, A, Kharbanda, R, Saeb-Parsy, K, Murphy, M, Frezza, C, Krieg, T, Channon, K, and Study, Oxford Acute Myocardial Infarction (Oxami)

Subjects
Adult, Male, Time Factors, Myocardial Biology, ischemia–reperfusion injury, Succinic Acid, Magnetic Resonance Imaging, Cine, Myocardial Reperfusion Injury, Coronary Angiography, myocardial metabolism, Percutaneous Coronary Intervention, Ischemia, Humans, Coronary Heart Disease, cardiovascular diseases, Aged, Retrospective Studies, Original Research, Aged, 80 and over, Myocardium, Middle Aged, Prognosis, mitochondria, myocardial ischemia, surgical procedures, operative, Metabolism, ST Elevation Myocardial Infarction, Female, Biomarkers, Basic Science Research, Follow-Up Studies
Abstract

Background Ischemia–reperfusion injury following ST‐segment–elevation myocardial infarction (STEMI) is a leading determinant of clinical outcome. In experimental models of myocardial ischemia, succinate accumulation leading to mitochondrial dysfunction is a major cause of ischemia–reperfusion injury; however, the potential importance and specificity of myocardial succinate accumulation in human STEMI is unknown. We sought to identify the metabolites released from the heart in patients undergoing primary percutaneous coronary intervention for emergency treatment of STEMI. Methods and Results Blood samples were obtained from the coronary artery, coronary sinus, and peripheral vein in patients undergoing primary percutaneous coronary intervention for acute STEMI and in control patients undergoing nonemergency coronary angiography or percutaneous coronary intervention for stable angina or non‐STEMI. Plasma metabolites were analyzed by targeted liquid chromatography and mass spectrometry. Metabolite levels for coronary artery, coronary sinus, and peripheral vein were compared to derive cardiac and systemic release ratios. In STEMI patients, cardiac magnetic resonance imaging was performed 2 days and 6 months after primary percutaneous coronary intervention to quantify acute myocardial edema and final infarct size, respectively. In total, 115 patients undergoing acute STEMI and 26 control patients were included. Succinate was the only metabolite significantly increased in coronary sinus blood compared with venous blood in STEMI patients, indicating cardiac release of succinate. STEMI patients had higher succinate concentrations in arterial, coronary sinus, and peripheral venous blood than patients with non‐STEMI or stable angina. Furthermore, cardiac succinate release in STEMI correlated with the extent of acute myocardial injury, quantified by cardiac magnetic resonance imaging. Conclusion Succinate release by the myocardium correlates with the extent of ischemia.

Published
2018
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19. Metabolic Reprogramming and Oncogenesis: One Hallmark, Many Organelles

Author

Costa, ASH, Frezza, C, Frezza, Christian [0000-0002-3293-7397], and Apollo - University of Cambridge Repository

Subjects
Organelle cross talk, Organelles, Metabolism, Cell Transformation, Neoplastic, Compartmentalization, Carcinogenesis, Neoplasms, Animals, Humans, Metabolic cooperation, Cancer, Cell Compartmentation
Abstract

The process of tumorigenesis can be described by a series of molecular features, among which alteration of cellular metabolism has recently emerged. This metabolic rewiring fulfills the energy and biosynthetic demands of fast proliferating cancer cells and amplifies their metabolic repertoire to survive and proliferate in the poorly oxygenated and nutrient-deprived tumor microenvironment. During the last decade, the complex reprogramming of cancer cell metabolism has been widely investigated, revealing cancer-specific metabolic alterations. These include dysregulation of glucose and glutamine metabolism, alterations of lipid synthesis and oxidation, and a complex rewiring of mitochondrial function. However, mitochondria are not the only metabolically active organelles within the cell, and other organelles, including lysosomes, peroxisomes, and endoplasmic reticulum, harbor components of the metabolic network. Of note, dysregulation of the function of these organelles is increasingly recognized in cancer cells. However, to what extent these organelles contribute to the metabolic reprogramming of cancer is not fully understood. In this review, we describe the main metabolic functions of these organelles and provide insights into how they communicate to orchestrate a coordinated metabolic reprogramming during transformation.

Published
2017

22. Succinate as a matabolic signature of ischaemia

Author

Kulaveerasingam, D., primary, Pell, V., additional, Kohlhauer, M., additional, Spiroski, A.M., additional, Young, T., additional, Costa, S., additional, Frezza, C., additional, Murphy, M., additional, and Krieg, T., additional

Published
2018
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23. Extracellular vesicles are independent metabolic units with asparaginase activity

Author

Iraci, N, Gaude, E, Leonardi, T, Costa, A, Cossetti, C, Peruzzotti Jametti, L, Bernstock, J, Saini, H, Gelati, M, Vescovi, A, Bastos, C, Faria, N, Occhipinti, L, Enright, A, Frezza, C, Pluchino, S, Costa, ASH, Bernstock, JD, Saini, HK, Vescovi, AL, Occhipinti, LG, Enright, AJ, Iraci, N, Gaude, E, Leonardi, T, Costa, A, Cossetti, C, Peruzzotti Jametti, L, Bernstock, J, Saini, H, Gelati, M, Vescovi, A, Bastos, C, Faria, N, Occhipinti, L, Enright, A, Frezza, C, Pluchino, S, Costa, ASH, Bernstock, JD, Saini, HK, Vescovi, AL, Occhipinti, LG, and Enright, AJ

Abstract

Extracellular vesicles (EVs) are membrane particles involved in the exchange of a broad range of bioactive molecules between cells and the microenvironment. Although it has been shown that cells can traffic metabolic enzymes via EVs, much remains to be elucidated with regard to their intrinsic metabolic activity. Accordingly, herein we assessed the ability of neural stem/progenitor cell (NSC)-derived EVs to consume and produce metabolites. Our metabolomics and functional analyses both revealed that EVs harbor L-asparaginase activity, catalyzed by the enzyme asparaginase-like protein 1 (Asrgl1). Critically, we show that Asrgl1 activity is selective for asparagine and is devoid of glutaminase activity. We found that mouse and human NSC EVs traffic Asrgl1. Our results demonstrate, for the first time, that NSC EVs function as independent metabolic units that are able to modify the concentrations of critical nutrients, with the potential to affect the physiology of their microenvironment.

Published
2017

24. Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

Author

Klionsky, D.J. Abdelmohsen, K. Abe, A. Abedin, M.J. Abeliovich, H. Arozena, A.A. Adachi, H. Adams, C.M. Adams, P.D. Adeli, K. Adhihetty, P.J. Adler, S.G. Agam, G. Agarwal, R. Aghi, M.K. Agnello, M. Agostinis, P. Aguilar, P.V. Aguirre-Ghiso, J. Airoldi, E.M. Ait-Si-Ali, S. Akematsu, T. Akporiaye, E.T. Al-Rubeai, M. Albaiceta, G.M. Albanese, C. Albani, D. Albert, M.L. Aldudo, J. Algül, H. Alirezaei, M. Alloza, I. Almasan, A. Almonte-Beceril, M. Alnemri, E.S. Alonso, C. Altan-Bonnet, N. Altieri, D.C. Alvarez, S. Alvarez-Erviti, L. Alves, S. Amadoro, G. Amano, A. Amantini, C. Ambrosio, S. Amelio, I. Amer, A.O. Amessou, M. Amon, A. An, Z. Anania, F.A. Andersen, S.U. Andley, U.P. Andreadi, C.K. Andrieu-Abadie, N. Anel, A. Ann, D.K. Anoopkumar-Dukie, S. Antonioli, M. Aoki, H. Apostolova, N. Aquila, S. Aquilano, K. Araki, K. Arama, E. Aranda, A. Araya, J. Arcaro, A. Arias, E. Arimoto, H. Ariosa, A.R. Armstrong, J.L. Arnould, T. Arsov, I. Asanuma, K. Askanas, V. Asselin, E. Atarashi, R. Atherton, S.S. Atkin, J.D. Attardi, L.D. Auberger, P. Auburger, G. Aurelian, L. Autelli, R. Avagliano, L. Avantaggiati, M.L. Avrahami, L. Azad, N. Awale, S. Bachetti, T. Backer, J.M. Bae, D.-H. Bae, J.-S. Bae, O.-N. Bae, S.H. Baehrecke, E.H. Baek, S.-H. Baghdiguian, S. Bagniewska-Zadworna, A. Bai, H. Bai, J. Bai, X.-Y. Bailly, Y. Balaji, K.N. Balduini, W. Ballabio, A. Balzan, R. Banerjee, R. Bánhegyi, G. Bao, H. Barbeau, B. Barrachina, M.D. Barreiro, E. Bartel, B. Bartolomé, A. Bassham, D.C. Bassi, M.T. Bast, R.C., Jr. Basu, A. Batista, M.T. Batoko, H. Battino, M. Bauckman, K. Baumgarner, B.L. Bayer, K.U. Beale, R. Beaulieu, J.-F. Beck, G.R., Jr. Becker, C. Beckham, J.D. Bédard, P.-A. Bednarski, P.J. Begley, T.J. Behl, C. Behrends, C. Behrens, G.M.N. Behrns, K.E. Bejarano, E. Belaid, A. Belleudi, F. Bénard, G. Berchem, G. Bergamaschi, D. Bergami, M. Berkhout, B. Berliocchi, L. Bernard, A. Bernard, M. Bernassola, F. Bertolotti, A. Bess, A.S. Besteiro, S. Bettuzzi, S. Bhalla, S. Bhattacharyya, S. Bhutia, S.K. Biagosch, C. Bianchi, M.W. Biard-Piechaczyk, M. Billes, V. Bincoletto, C. Bingol, B. Bird, S.W. Bitoun, M. Bjedov, I. Blackstone, C. Blanc, L. Blanco, G.A. Blomhoff, H.K. Boada-Romero, E. Böckler, S. Boes, M. Boesze-Battaglia, K. Boise, L.H. Bolino, A. Boman, A. Bonaldo, P. Bordi, M. Bosch, J. Botana, L.M. Botti, J. Bou, G. Bouché, M. Bouchecareilh, M. Boucher, M.-J. Boulton, M.E. Bouret, S.G. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N. Braga, V.M.M. Brancolini, C. Braus, G.H. Bravo-San-Pedro, J.M. Brennan, L.A. Bresnick, E.H. Brest, P. Bridges, D. Bringer, M.-A. Brini, M. Brito, G.C. Brodin, B. Brookes, P.S. Brown, E.J. Brown, K. Broxmeyer, H.E. Bruhat, A. Brum, P.C. Brumell, J.H. Brunetti-Pierri, N. Bryson-Richardson, R.J. Buch, S. Buchan, A.M. Budak, H. Bulavin, D.V. Bultman, S.J. Bultynck, G. Bumbasirevic, V. Burelle, Y. Burke, R.E. Burmeister, M. Bütikofer, P. Caberlotto, L. Cadwell, K. Cahova, M. Cai, D. Cai, J. Cai, Q. Calatayud, S. Camougrand, N. Campanella, M. Campbell, G.R. Campbell, M. Campello, S. Candau, R. Caniggia, I. Cantoni, L. Cao, L. Caplan, A.B. Caraglia, M. Cardinali, C. Cardoso, S.M. Carew, J.S. Carleton, L.A. Carlin, C.R. Carloni, S. Carlsson, S.R. Carmona-Gutierrez, D. Carneiro, L.A.M. Carnevali, O. Carra, S. Carrier, A. Carroll, B. Casas, C. Casas, J. Cassinelli, G. Castets, P. Castro-Obregon, S. Cavallini, G. Ceccherini, I. Cecconi, F. Cederbaum, A.I. Ceña, V. Cenci, S. Cerella, C. Cervia, D. Cetrullo, S. Chaachouay, H. Chae, H.-J. Chagin, A.S. Chai, C.-Y. Chakrabarti, G. Chamilos, G. Chan, E.Y.W. Chan, M.T.V. Chandra, D. Chandra, P. Chang, C.-P. Chang, R.C.-C. Chang, T.Y. Chatham, J.C. Chatterjee, S. Chauhan, S. Che, Y. Cheetham, M.E. Cheluvappa, R. Chen, C.-J. Chen, G. Chen, G.-C. Chen, G. Chen, H. Chen, J.W. Chen, J.-K. Chen, M. Chen, M. Chen, P. Chen, Q. Chen, Q. Chen, S.-D. Chen, S. Chen, S.S.-L. Chen, W. Chen, W.-J. Chen, W.Q. Chen, W. Chen, X. Chen, Y.-H. Chen, Y.-G. Chen, Y. Chen, Y. Chen, Y. Chen, Y.-J. Chen, Y.-Q. Chen, Y. Chen, Z. Chen, Z. Cheng, A. Cheng, C.H.K. Cheng, H. Cheong, H. Cherry, S. Chesney, J. Cheung, C.H.A. Chevet, E. Chi, H.C. Chi, S.-G. Chiacchiera, F. Chiang, H.-L. Chiarelli, R. Chiariello, M. Chieppa, M. Chin, L.-S. Chiong, M. Chiu, G.N.C. Cho, D.-H. Cho, S.-G. Cho, W.C. Cho, Y.-Y. Cho, Y.-S. Choi, A.M.K. Choi, E.-J. Choi, E.-K. Choi, J. Choi, M.E. Choi, S.-I. Chou, T.-F. Chouaib, S. Choubey, D. Choubey, V. Chow, K.-C. Chowdhury, K. Chu, C.T. Chuang, T.-H. Chun, T. Chung, H. Chung, T. Chung, Y.-L. Chwae, Y.-J. Cianfanelli, V. Ciarcia, R. Ciechomska, I.A. Ciriolo, M.R. Cirone, M. Claerhout, S. Clague, M.J. Cl� ria, J. Clarke, P.G.H. Clarke, R. Clementi, E. Cleyrat, C. Cnop, M. Coccia, E.M. Cocco, T. Codogno, P. Coers, J. Cohen, E.E.W. Colecchia, D. Coletto, L. Coll, N.S. Colucci-Guyon, E. Comincini, S. Condello, M. Cook, K.L. Coombs, G.H. Cooper, C.D. Cooper, J.M. Coppens, I. Corasaniti, M.T. Corazzari, M. Corbalan, R. Corcelle-Termeau, E. 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Published
2016

25. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy

Author

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Published
2016

26. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Author

Klionsky, D.J. Abdelmohsen, K. Abe, A. Abedin, M.J. Abeliovich, H. Arozena, A.A. Adachi, H. Adams, C.M. Adams, P.D. Adeli, K. Adhihetty, P.J. Adler, S.G. Agam, G. Agarwal, R. Aghi, M.K. Agnello, M. Agostinis, P. Aguilar, P.V. Aguirre-Ghiso, J. Airoldi, E.M. Ait-Si-Ali, S. Akematsu, T. Akporiaye, E.T. Al-Rubeai, M. Albaiceta, G.M. Albanese, C. Albani, D. Albert, M.L. Aldudo, J. Algül, H. Alirezaei, M. Alloza, I. Almasan, A. Almonte-Beceril, M. Alnemri, E.S. Alonso, C. Altan-Bonnet, N. Altieri, D.C. Alvarez, S. Alvarez-Erviti, L. Alves, S. Amadoro, G. Amano, A. Amantini, C. Ambrosio, S. Amelio, I. Amer, A.O. Amessou, M. Amon, A. An, Z. Anania, F.A. Andersen, S.U. Andley, U.P. Andreadi, C.K. Andrieu-Abadie, N. Anel, A. Ann, D.K. Anoopkumar-Dukie, S. Antonioli, M. Aoki, H. Apostolova, N. Aquila, S. Aquilano, K. Araki, K. Arama, E. Aranda, A. Araya, J. Arcaro, A. Arias, E. Arimoto, H. Ariosa, A.R. Armstrong, J.L. Arnould, T. Arsov, I. Asanuma, K. Askanas, V. Asselin, E. Atarashi, R. 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Published
2016

27. Testing anti-HIV activity of antiretroviral agents in vitro using flow cytometry analysis of CEM-GFP cells infected with transfection-derived HIV-1 NL4-3

Author

Frezza, C, Grelli, S, Federico, M, Marino Merlo, F, Mastino, A, and Macchi, B

Subjects
anti-HIV assay, antiviral drugs, drug resistance, green fluorescent protein (GFP), human immunodeficiency virus type 1 (HIV-1), Anti-HIV Agents, Cell Survival, viruses, HIV Core Protein p24, Microbial Sensitivity Tests, Transfection, Inhibitory Concentration 50, immune system diseases, Anti-HIV assay, Cell Line, Tumor, Humans, Nevirapine, Human immunodeficiency virus type 1 (HIV-1), Antiviral drugs, Drug resistance, Green fluorescent protein (GFP), Virology, Infectious Diseases, Settore BIO/14, virus diseases, biochemical phenomena, metabolism, and nutrition, Settore MED/07 - Microbiologia e Microbiologia Clinica, Flow Cytometry, HEK293 Cells, HIV-1, Zidovudine
Abstract

An assay, specifically optimized to evaluate the anti-HIV activity of antiretrovirals by flow cytometry analysis, is described. As widely used anti-HIV agents, zidovudine (AZT), abaca- vir (ABC), 20,30-dideoxyinosine (DDI), lamivu-dine (3TC), nevirapine (NVP), and efavirenz (EFV), and as drugs of recent approval raltegra- vir (RAL), etravirine (ETR), and rilpivirine (RPV), were utilized as reference drugs. HIV-1 NL4-3 virus was prepared by transfection of HEK293T cells with purified plasmid DNA and quantified by p24 antigen-capture assay. For infection, CEM-GFP cells were exposed to vehicle or to several concentrations of the drugs for 2 hr at 37°C before HIV-1 NL4-3 was added to each sample. The adsorption was prolonged for 3 hr at 37°C. After 72 hr of incubation, HIV-induced GFP expression in infected CEM-GFP cells was assessed by flow cytometry analysis and expressed as % positive cells. For comparison, p24 production in supernatants was assessed by a commercial ELISA kit. On the basis of IC50 values, the anti-HIV activity, as assayed by this method, was EFV>3TC>AZT>NVP>DDI> ABC and ETR>RPV>RAL. The comparison between the IC50 values calculated through flow cytometry and p24 production revealed overlapping results, showing that the opti- mized protocol of CEM-GFP infection with HIV NL4-3 is a suitable method to perform quanti-tative, rapid and low-expensive screening tests to evaluate the in vitro effect of new candidate anti-HIV drugs.

Published
2016
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28. Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

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Robin, Higaki, Katsumi, Hilfiker, Sabine, Hill, Bradford G., Hill, Joseph A., Hill, William D., Hino, Keisuke, Hofius, Daniel, Hofman, Paul, Höglinger, Günter U., Höhfeld, Jörg, Holz, Marina K., Hong, Yonggeun, Hood, David A., Hoozemans, Jeroen J.M., Hoppe, Thorsten, Hsu, Chin, Hsu, Chin-Yuan, Hsu, Li-Chung, Hu, Dong, Hu, Guochang, Hu, Hong-Ming, Hu, Hongbo, Hu, Ming Chang, Hu, Yu-Chen, Hu, Zhuo-Wei, Hua, Fang, Hua, Ya, Huang, Canhua, Huang, Huey-Lan, Huang, Kuo-How, Huang, Kuo-Yang, Huang, Shile, Huang, Shiqian, Huang, Wei-Pang, Huang, Yi-Ran, Huang, Yong, Huang, Yunfei, Huber, Tobias B., Huebbe, Patricia, Huh, Won-Ki, Hulmi, Juha J., Hur, Gang Min, Hurley, James H., Husak, Zvenyslava, Hussain, Sabah N.A., Hussain, Salik, Hwang, Jung Jin, Hwang, Seungmin, Hwang, Thomas I.S., Ichihara, Atsuhiro, Imai, Yuzuru, Imbriano, Carol, Inomata, Megumi, Into, Takeshi, Iovane, Valentina, Iovanna, Juan L., Iozzo, Renato V., Ip, Nancy Y., Irazoqui, Javier E., Iribarren, Pablo, Isaka, Yoshitaka, Isakovic, Aleksandra J., Ischiropoulos, Harry, Isenberg, Jeffrey S., Ishaq, Mohammad, Ishida, Hiroyuki, Ishii, Isao, Ishmael, Jane E., Isidoro, Ciro, Isobe, Ken-Ichi, Isono, Erika, Issazadeh-Navikas, Shohreh, Itahana, Koji, Itakura, Eisuke, Ivanov, Andrei I., Iyer, Anand Krishnan V., Izquierdo, José M., Izumi, Yotaro, Izzo, Valentina, Jäättelä, Marja, Jaber, Nadia, Jackson, Daniel John, Jackson, William T., Jacob, Tony George, Jacques, Thomas S., Jagannath, Chinnaswamy, Jain, Ashish, Jana, Nihar Ranjan, Jang, Byoung Kuk, Jani, Alkesh, Janji, Bassam, Jannig, Paulo Roberto, Jansson, Patric J., Jean, Steve, Jendrach, Marina, Jeon, Ju-Hong, Jessen, Niel, Jeung, Eui-Bae, Jia, Kailiang, Jia, Lijun, Jiang, Hong, Jiang, Hongchi, Jiang, Liwen, Jiang, Teng, Jiang, Xiaoyan, Jiang, Xuejun, Jiang, Ying, Jiang, Yongjun, Jiménez, Alberto, Jin, Cheng, Jin, Hongchuan, Jin, Lei, Jin, Meiyan, Jin, Shengkan, Jinwal, Umesh Kumar, Jo, Eun-Kyeong, Johansen, Terje, Johnson, Daniel E., Johnson, Gail V.W., Johnson, James D., Jonasch, Eric, Jones, Chri, Joosten, Leo A.B., Jordan, Joaquin, Joseph, Anna-Maria, Joseph, Bertrand, Joubert, Annie M., Ju, Dianwen, Ju, Jingfang, Juan, Hsueh-Fen, Juenemann, Katrin, Juhász, Gábor, Jung, Hye Seung, Jung, Jae U., Jung, Yong-Keun, Jungbluth, Heinz, Justice, Matthew J., Jutten, Barry, Kaakoush, Nadeem O., Kaarniranta, Kai, Kaasik, Allen, Kabuta, Tomohiro, Kaeffer, Bertrand, Kågedal, Katarina, Kahana, Alon, Kajimura, Shingo, Kakhlon, Or, Kalia, Manjula, Kalvakolanu, Dhan V., Kamada, Yoshiaki, Kambas, Konstantino, Kaminskyy, Vitaliy O., Kampinga, Harm H., Kandouz, Mustapha, Kang, Chanhee, Kang, Rui, Kang, Tae-Cheon, Kanki, Tomotake, Kanneganti, Thirumala-Devi, Kanno, Haruo, Kanthasamy, Anumantha G., Kantorow, Marc, Kaparakis-Liaskos, Maria, Kapuy, Orsolya, Karantza, Vassiliki, Karim, Md Razaul, Karmakar, Parimal, Kaser, Arthur, Kaushik, Susmita, Kawula, Thoma, Kaynar, A. Murat, Ke, Po-Yuan, Ke, Zun-Ji, Kehrl, John H., Keller, Kate E., Kemper, Jongsook Kim, Kenworthy, Anne K., Kepp, Oliver, Kern, Andrea, Kesari, Santosh, Kessel, David, Ketteler, Robin, Kettelhut, Isis do Carmo, Khambu, Bilon, Khan, Muzamil Majid, Khandelwal, Vinoth K.M., Khare, Sangeeta, Kiang, Juliann G., Kiger, Amy A., Kihara, Akio, Kim, Arianna L., Kim, Cheol Hyeon, Kim, Deok Ryong, Kim, Do-Hyung, Kim, Eung Kweon, Kim, Hye Young, Kim, Hyung-Ryong, Kim, Jae-Sung, Kim, Jeong Hun, Kim, Jin Cheon, Kim, Jin Hyoung, Kim, Kwang Woon, Kim, Michael D., Kim, Moon-Moo, Kim, Peter K., Kim, Seong Who, Kim, Soo-Youl, Kim, Yong-Sun, Kim, Yonghyun, Kimchi, Adi, Kimmelman, Alec C., Kimura, Tomonori, King, Jason S., Kirkegaard, Karla, Kirkin, Vladimir, Kirshenbaum, Lorrie A., Kishi, Shuji, Kitajima, Yasuo, Kitamoto, Katsuhiko, Kitaoka, Yasushi, Kitazato, Kaio, Kley, Rudolf A., Klimecki, Walter T., Klinkenberg, Michael, Klucken, Jochen, Knævelsrud, Helene, Knecht, Erwin, Knuppertz, Laura, Ko, Jiunn-Liang, Kobayashi, Satoru, Koch, Jan C., Koechlin-Ramonatxo, Christelle, Koenig, Ulrich, Koh, Young Ho, Köhler, Katja, Kohlwein, Sepp D., Koike, Masato, Komatsu, Masaaki, Kominami, Eiki, Kong, Dexin, Kong, Hee Jeong, Konstantakou, Eumorphia G., Kopp, Benjamin T., Korcsmaros, Tama, Korhonen, Laura, Korolchuk, Viktor I., Koshkina, Nadya V., Kou, Yanjun, Koukourakis, Michael I., Koumenis, Constantino, Kovács, Attila L., Kovács, Tibor, Kovacs, Werner J., Koya, Daisuke, Kraft, Claudine, Krainc, Dimitri, Kramer, Helmut, Kravic-Stevovic, Tamara, Krek, Wilhelm, Kretz-Remy, Carole, Krick, Roswitha, Krishnamurthy, Malathi, Kriston-Vizi, Jano, Kroemer, Guido, Kruer, Michael C., Kruger, Rejko, Ktistakis, Nicholas T., Kuchitsu, Kazuyuki, Kuhn, Christian, Kumar, Addanki Pratap, Kumar, Anuj, Kumar, Ashok, Kumar, Deepak, Kumar, Dhiraj, Kumar, Rakesh, Kumar, Sharad, Kundu, Mondira, Kung, Hsing-Jien, Kuno, Atsushi, Kuo, Sheng-Han, Kuret, Jeff, Kurz, Tino, Kwok, Terry, Kwon, Taeg Kyu, Kwon, Yong Tae, Kyrmizi, Irene, La Spada, Albert R., Lafont, Frank, Lahm, Tim, Lakkaraju, Aparna, Lam, Truong, Lamark, Trond, Lancel, Steve, Landowski, Terry H., Lane, Darius J.R., Lane, Jon D., Lanzi, Cinzia, Lapaquette, Pierre, Lapierre, Louis R., Laporte, Jocelyn, Laukkarinen, Johanna, Laurie, Gordon W., Lavandero, Sergio, Lavie, Lena, Lavoie, Matthew J., Law, Betty Yuen Kwan, Law, Helen Ka-Wai, Law, Kelsey B., Layfield, Robert, Lazo, Pedro A., Le Cam, Laurent, Le Roch, Karine G., Le Stunff, Hervé, Leardkamolkarn, Vijittra, Lecuit, Marc, Lee, Byung-Hoon, Lee, Che-Hsin, Lee, Erinna F., Lee, Gyun Min, Lee, He-Jin, Lee, Hsinyu, Lee, Jae Keun, Lee, Jongdae, Lee, Ju-Hyun, Lee, Jun Hee, Lee, Michael, Lee, Myung-Shik, Lee, Patty J., Lee, Sam W., Lee, Seung-Jae, Lee, Shiow-Ju, Lee, Stella Y., Lee, Sug Hyung, Lee, Sung Sik, Lee, Sung-Joon, Lee, Sunhee, Lee, Ying-Ray, Lee, Yong J., Lee, Young H., Leeuwenburgh, Christiaan, Lefort, Sylvain, Legouis, Renaud, Lei, Jinzhi, Lei, Qun-Ying, Leib, David A., Leibowitz, Gil, Lekli, Istvan, Lemaire, Stéphane D., Lemasters, John J., Lemberg, Marius K., Lemoine, Antoinette, Leng, Shuilong, Lenz, Guido, Lenzi, Paola, Lerman, Lilach O., Barbato, Daniele Lettieri, Leu, Julia I. 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Sue, Menna-Barreto, Rubem F.S., Menon, Manoj B., Meraz-Ríos, Marco A., Merla, Giuseppe, Merlini, Luciano, Merlot, Angelica M., Meryk, Andrea, Meschini, Stefania, Meyer, Joel N., Mi, Man-Tian, Miao, Chao-Yu, Micale, Lucia, Michaeli, Simon, Michiels, Carine, Migliaccio, Anna Rita, Mihailidou, Anastasia Susie, Mijaljica, Dalibor, Mikoshiba, Katsuhiko, Milan, Enrico, Miller-Fleming, Leonor, Mills, Gordon B., Mills, Ian G., Minakaki, Georgia, Minassian, Berge A., Ming, Xiu-Fen, Minibayeva, Farida, Minina, Elena A., Mintern, Justine D., Minucci, Saverio, Miranda-Vizuete, Antonio, Mitchell, Claire H., Miyamoto, Shigeki, Miyazawa, Keisuke, Mizushima, Noboru, Mnich, Katarzyna, Mograbi, Baharia, Mohseni, Simin, Moita, Luis Ferreira, Molinari, Marco, Molinari, Maurizio, Møller, Andreas Buch, Mollereau, Bertrand, Mollinedo, Faustino, Mongillo, Marco, Monick, Martha M., Montagnaro, Serena, Montell, Craig, Moore, Darren J., Moore, Michael N., Mora-Rodriguez, Rodrigo, Moreira, Paula I., Morel, Etienne, Morelli, Maria Beatrice, Moreno, Sandra, Morgan, Michael J., Moris, Arnaud, Moriyasu, Yuji, Morrison, Janna L., Morrison, Lynda A., Morselli, Eugenia, Moscat, Jorge, Moseley, Pope L., Mostowy, Serge, Motori, Elisa, Mottet, Deni, Mottram, Jeremy C., Moussa, Charbel E.-H., Mpakou, Vassiliki E., Mukhtar, Hasan, Levy, Jean M. Mulcahy, Muller, Sylviane, Muñoz-Moreno, Raquel, Muñoz-Pinedo, Cristina, Münz, Christian, Murphy, Maureen E., Murray, James T., Murthy, Aditya, Mysorekar, Indira U., Nabi, Ivan R., Nabissi, Massimo, Nader, Gustavo A., Nagahara, Yukitoshi, Nagai, Yoshitaka, Nagata, Kazuhiro, Nagelkerke, Anika, Nagy, Péter, Naidu, Samisubbu R., Nair, Sreejayan, Nakano, Hiroyasu, Nakatogawa, Hitoshi, Nanjundan, Meera, Napolitano, Gennaro, Naqvi, Naweed I., Nardacci, Roberta, Narendra, Derek P., Narita, Masashi, Nascimbeni, Anna Chiara, Natarajan, Ramesh, Navegantes, Luiz C., Nawrocki, Steffan T., Nazarko, Taras Y., Nazarko, Volodymyr Y., Neill, Thoma, Neri, Luca M., Netea, Mihai G., Netea-Maier, Romana T., Neves, Bruno M., Ney, Paul A., Nezis, Ioannis P., Nguyen, Hang T.T., Nguyen, Huu Phuc, Nicot, Anne-Sophie, Nilsen, Hilde, Nilsson, Per, Nishimura, Mikio, Nishino, Ichizo, Niso-Santano, Mireia, Niu, Hua, Nixon, Ralph A., Njar, Vincent C.O., Noda, Takeshi, Noegel, Angelika A., Nolte, Elsie Magdalena, Norberg, Erik, Norga, Koenraad K., Noureini, Sakineh Kazemi, Notomi, Shoji, Notterpek, Lucia, Nowikovsky, Karin, Nukina, Nobuyuki, Nürnberger, Thorsten, O'donnell, Valerie B., O'donovan, Tracey, O'dwyer, Peter J., Oehme, Ina, Oeste, Clara L., Ogawa, Michinaga, Ogretmen, Besim, Ogura, Yuji, Oh, Young J., Ohmuraya, Masaki, Ohshima, Takayuki, Ojha, Rani, Okamoto, Koji, Okazaki, Toshiro, Oliver, F. Javier, Ollinger, Karin, Olsson, Stefan, Orban, Daniel P., Ordonez, Paulina, Orhon, Idil, Orosz, Laszlo, O'rourke, Eyleen J., Orozco, Helena, Ortega, Angel L., Ortona, Elena, Osellame, Laura D., Oshima, Junko, Oshima, Shigeru, Osiewacz, Heinz D., Otomo, Takanobu, Otsu, Kinya, Ou, Jing-Hsiung Jame, Outeiro, Tiago F., Ouyang, Dong-Yun, Ouyang, Hongjiao, Overholtzer, Michael, Ozbun, Michelle A., Ozdinler, P. Hande, Ozpolat, Bulent, Pacelli, Consiglia, Paganetti, Paolo, Page, Guyléne, Pages, Gille, Pagnini, Ugo, Pajak, Beata, Pak, Stephen C., Pakos-Zebrucka, Karolina, Pakpour, Nazzy, Palková, Zdena, Palladino, Francesca, Pallauf, Kathrin, Pallet, Nicola, Palmieri, Marta, Paludan, Søren R., Palumbo, Camilla, Palumbo, Silvia, Pampliega, Olatz, Pan, Hongming, Pan, Wei, Panaretakis, Theochari, Pandey, Aseem, Pantazopoulou, Areti, Papackova, Zuzana, Papademetrio, Daniela L., Papassideri, Issidora, Papini, Alessio, Parajuli, Nirmala, Pardo, Julian, Parekh, Vrajesh V., Parenti, Giancarlo, Park, Jong-In, Park, Junsoo, Park, Ohkmae K., Parker, Roy, Parlato, Rosanna, Parys, Jan B., Parzych, Katherine R., Pasquet, Jean-Max, Pasquier, Benoit, Pasumarthi, Kishore B.S., Patschan, Daniel, Pattingre, Sophie, Pattison, Scott, Pause, Arnim, Pavenstädt, Hermann, Pavone, Flaminia, Pedrozo, Zully, Peña, Fernando J., Peñalva, Miguel A., Pende, Mario, Peng, Jianxin, Penna, Fabio, Penninger, Josef M., Pensalfini, Anna, Pepe, Salvatore, Pereira, Gustavo J.S., Pereira, Paulo C., de la Cruz, Verónica Pérez, Pérez-Pérez, María Esther, Pérez-Rodríguez, Diego, Pérez-Sala, Dolore, Perier, Celine, Perl, Andra, Perlmutter, David H., Perrotta, Ida, Pervaiz, Shazib, Pesonen, Maija, Pessin, Jeffrey E., Peters, Godefridus J., Petersen, Morten, Petrache, Irina, Petrof, Basil J., Petrovski, Goran, Phang, James M., Piacentini, Mauro, Pierdominici, Marina, Pierre, Philippe, Pierrefite-Carle, Valérie, Pietrocola, Federico, Pimentel-Muiños, Felipe X., Pinar, Mario, Pineda, Benjamin, Pinkas-Kramarski, Ronit, Pinti, Marcello, Pinton, Paolo, Piperdi, Bilal, Piret, James M., Platanias, Leonidas C., Platta, Harald W., Plowey, Edward D., Pöggeler, Stefanie, Poirot, Marc, Polčic, Peter, Poletti, Angelo, Poon, Audrey H., Popelka, Hana, Popova, Blagovesta, Poprawa, Izabela, Poulose, Shibu M., Poulton, Joanna, Powers, Scott K., Powers, Ted, Pozuelo-Rubio, Mercede, Prak, Krisna, Prange, Reinhild, Prescott, Mark, Priault, Muriel, Prince, Sharon, Proia, Richard L., Proikas-Cezanne, Tassula, Prokisch, Holger, Promponas, Vasilis J., Przyklenk, Karin, Puertollano, Rosa, Pugazhenthi, Subbiah, Puglielli, Luigi, Pujol, Aurora, Puyal, Julien, Pyeon, Dohun, Qi, Xin, Qian, Wen-Bin, Qin, Zheng-Hong, Qiu, Yu, Qu, Ziwei, Quadrilatero, Joe, Quinn, Frederick, Raben, Nina, Rabinowich, Hannah, Radogna, Flavia, Ragusa, Michael J., Rahmani, Mohamed, Raina, Komal, Ramanadham, Sasanka, Ramesh, Rajagopal, Rami, Abdelhaq, Randall-Demllo, Sarron, Randow, Felix, Rao, Hai, Rao, V. Ashutosh, Rasmussen, Blake B., Rasse, Tobias M., Ratovitski, Edward A., Rautou, Pierre-Emmanuel, Ray, Swapan K., Razani, Babak, Reed, Bruce H., Reggiori, Fulvio, Rehm, Marku, Reichert, Andreas S., Rein, Theo, Reiner, David J., Reits, Eric, Ren, Jun, Ren, Xingcong, Renna, Maurizio, Reusch, Jane E.B., Revuelta, Jose L., Reyes, Leticia, Rezaie, Alireza R., Richards, Robert I., Richardson, Des R., Richetta, Clémence, Riehle, Michael A., Rihn, Bertrand H., Rikihisa, Yasuko, Riley, Brigit E., Rimbach, Gerald, Rippo, Maria Rita, Ritis, Konstantino, Rizzi, Federica, Rizzo, Elizete, Roach, Peter J., Robbins, Jeffrey, Roberge, Michel, Roca, Gabriela, Roccheri, Maria Carmela, Rocha, Sonia, Rodrigues, Cecilia M.P., Rodríguez, Clara I., de Cordoba, Santiago Rodriguez, Rodriguez-Muela, Natalia, Roelofs, Jeroen, Rogov, Vladimir V., Rohn, Troy T., Rohrer, Bärbel, Romanelli, Davide, Romani, Luigina, Romano, Patricia Silvia, Roncero, M. Isabel G., Rosa, Jose Lui, Rosello, Alicia, Rosen, Kirill V., Rosenstiel, Philip, Rost-Roszkowska, Magdalena, Roth, Kevin A., Roué, Gael, Rouis, Mustapha, Rouschop, Kasper M., Ruan, Daniel T., Ruano, Diego, Rubinsztein, David C., Rucker, Edmund B., Rudich, Assaf, Rudolf, Emil, Rudolf, Ruediger, Ruegg, Markus A., Ruiz-Roldan, Carmen, Ruparelia, Avnika Ashok, Rusmini, Paola, Russ, David W., Russo, Gian Luigi, Russo, Giuseppe, Russo, Rossella, Rusten, Tor Erik, Ryabovol, Victoria, Ryan, Kevin M., Ryter, Stefan W., Sabatini, David M., Sacher, Michael, Sachse, Carsten, Sack, Michael N., Sadoshima, Junichi, Saftig, Paul, Sagi-Eisenberg, Ronit, Sahni, Sumit, Saikumar, Pothana, Saito, Tsunenori, Saitoh, Tatsuya, Sakakura, Koichi, Sakoh-Nakatogawa, Machiko, Sakuraba, Yasuhito, Salazar-Roa, María, Salomoni, Paolo, Saluja, Ashok K., Salvaterra, Paul M., Salvioli, Rosa, Samali, Afshin, Sanchez, Anthony M.J., Sánchez-Alcázar, José A., Sanchez-Prieto, Ricardo, Sandri, Marco, Sanjuan, Miguel A., Santaguida, Stefano, Santambrogio, Laura, Santoni, Giorgio, Dos Santos, Claudia Nune, Saran, Shweta, Sardiello, Marco, Sargent, Graeme, Sarkar, Pallabi, Sarkar, Sovan, Sarrias, Maria Rosa, Sarwal, Minnie M., Sasakawa, Chihiro, Sasaki, Motoko, Sass, Miklo, Sato, Ken, Sato, Miyuki, Satriano, Joseph, Savaraj, Niramol, Saveljeva, Svetlana, Schaefer, Liliana, Schaible, Ulrich E., Scharl, Michael, Schatzl, Hermann M., Schekman, Randy, Scheper, Wiep, Schiavi, Alfonso, Schipper, Hyman M., Schmeisser, Hana, Schmidt, Jen, Schmitz, Ingo, Schneider, Bianca E., Schneider, E. Marion, Schneider, Jaime L., Schon, Eric A., Schönenberger, Miriam J., Schönthal, Axel H., Schorderet, Daniel F., Schröder, Bernd, Schuck, Sebastian, Schulze, Ryan J., Schwarten, Melanie, Schwarz, Thomas L., Sciarretta, Sebastiano, Scotto, Kathleen, Scovassi, A. Ivana, Screaton, Robert A., Screen, Mark, Seca, Hugo, Sedej, Simon, Segatori, Laura, Segev, Nava, Seglen, Per O., Seguí-Simarro, Jose M., Segura-Aguilar, Juan, Seiliez, Iban, Seki, Ekihiro, Sell, Christian, Semenkovich, Clay F., Semenza, Gregg L., Sen, Utpal, Serra, Andreas L., Serrano-Puebla, Ana, Sesaki, Hiromi, Setoguchi, Takao, Settembre, Carmine, Shacka, John J., Shajahan-Haq, Ayesha N., Shapiro, Irving M., Sharma, Shweta, She, Hua, Shen, C.-K. Jame, Shen, Chiung-Chyi, Shen, Han-Ming, Shen, Sanbing, Shen, Weili, Sheng, Rui, Sheng, Xianyong, Sheng, Zu-Hang, Shepherd, Trevor G., Shi, Junyan, Shi, Qiang, Shi, Qinghua, Shi, Yuguang, Shibutani, Shusaku, Shibuya, Kenichi, Shidoji, Yoshihiro, Shieh, Jeng-Jer, Shih, Chwen-Ming, Shimada, Yohta, Shimizu, Shigeomi, Shin, Dong Wook, Shinohara, Mari L., Shintani, Michiko, Shintani, Takahiro, Shioi, Tetsuo, Shirabe, Ken, Shiri-Sverdlov, Ronit, Shirihai, Orian, Shore, Gordon C., Shu, Chih-Wen, Shukla, Deepak, Sibirny, Andriy A., Sica, Valentina, Sigurdson, Christina J., Sigurdsson, Einar M., Sijwali, Puran Singh, Sikorska, Beata, Silveira, Wilian A., Silvente-Poirot, Sandrine, Silverman, Gary A., Simak, Jan, Simmet, Thoma, Simon, Anna Katharina, Simon, Hans-Uwe, Simone, Cristiano, Simons, Matia, Simonsen, Anne, Singh, Rajat, Singh, Shivendra V., Singh, Shrawan K., Sinha, Debasish, Sinha, Sangita, Sinicrope, Frank A., Sirko, Agnieszka, Sirohi, Kapil, Sishi, Balindiwe J.N., Sittler, Annie, Siu, Parco M., Sivridis, Efthimio, Skwarska, Anna, Slack, Ruth, Slaninová, Iva, Slavov, Nikolai, Smaili, Soraya S., Smalley, Keiran S.M., Smith, Duncan R., Soenen, Stefaan J., Soleimanpour, Scott A., Solhaug, Anita, Somasundaram, Kumaravel, Son, Jin H., Sonawane, Avinash, Song, Chunjuan, Song, Fuyong, Song, Hyun Kyu, Song, Ju-Xian, Song, Wei, Soo, Kai Y., Sood, Anil K., Soong, Tuck Wah, Soontornniyomkij, Virawudh, Sorice, Maurizio, Sotgia, Federica, Soto-Pantoja, David R., Sotthibundhu, Areechun, Sousa, Maria João, Spaink, Herman P., Span, Paul N., Spang, Anne, Sparks, Janet D., Speck, Peter G., Spector, Stephen A., Spies, Claudia D., Springer, Wolfdieter, Clair, Daret St, Stacchiotti, Alessandra, Staels, Bart, Stang, Michael T., Starczynowski, Daniel T., Starokadomskyy, Petro, Steegborn, Clemen, Steele, John W., Stefanis, Leonida, Steffan, Joan, Stellrecht, Christine M., Stenmark, Harald, Stepkowski, Tomasz M., Stern, Stęphan T., Stevens, Craig, Stockwell, Brent R., Stoka, Veronika, Storchova, Zuzana, Stork, Björn, Stratoulias, Vassili, Stravopodis, Dimitrios J., Strnad, Pavel, Strohecker, Anne Marie, Ström, Anna-Lena, Stromhaug, Per, Stulik, Jiri, Su, Yu-Xiong, Su, Zhaoliang, Subauste, Carlos S., Subramaniam, Srinivasa, Sue, Carolyn M., Suh, Sang Won, Sui, Xinbing, Sukseree, Supawadee, Sulzer, David, Sun, Fang-Lin, Sun, Jiaren, Sun, Jun, Sun, Shi-Yong, Sun, Yang, Sun, Yi, Sun, Yingjie, Sundaramoorthy, Vinod, Sung, Joseph, Suzuki, Hidekazu, Suzuki, Kuninori, Suzuki, Naoki, Suzuki, Tadashi, Suzuki, Yuichiro J., Swanson, Michele S., Swanton, Charle, Swärd, Karl, Swarup, Ghanshyam, Sweeney, Sean T., Sylvester, Paul W., Szatmari, Zsuzsanna, Szegezdi, Eva, Szlosarek, Peter W., Taegtmeyer, Heinrich, Tafani, Marco, Taillebourg, Emmanuel, Tait, Stephen W.G., Takacs-Vellai, Krisztina, Takahashi, Yoshinori, Takáts, Szabolc, Takemura, Genzou, Takigawa, Nagio, Talbot, Nicholas J., Tamagno, Elena, Tamburini, Jerome, Tan, Cai-Ping, Tan, Lan, Tan, Mei Lan, Tan, Ming, Tan, Yee-Joo, Tanaka, Keiji, Tanaka, Masaki, Tang, Daolin, Tang, Dingzhong, Tang, Guomei, Tanida, Isei, Tanji, Kunikazu, Tannous, Bakhos A., Tapia, Jose A., Tasset-Cuevas, Inmaculada, Tatar, Marc, Tavassoly, Iman, Tavernarakis, Nektario, Taylor, Allen, Taylor, Graham S., Taylor, Gregory A., Taylor, J. Paul, Taylor, Mark J., Tchetina, Elena V., Tee, Andrew R., Teixeira-Clerc, Fatima, Telang, Sucheta, Tencomnao, Tewin, Teng, Ba-Bie, Teng, Ru-Jeng, Terro, Faraj, Tettamanti, Gianluca, Theiss, Arianne L., Theron, Anne E., Thomas, Kelly Jean, Thomé, Marcos P., Thomes, Paul G., Thorburn, Andrew, Thorner, Jeremy, Thum, Thoma, Thumm, Michael, Thurston, Teresa L.M., Tian, Ling, Till, Andrea, Ting, Jenny Pan-Yun, Ting, Jenny Pan Yun, Titorenko, Vladimir I., Toker, Lilach, Toldo, Stefano, Tooze, Sharon A., Topisirovic, Ivan, Torgersen, Maria Lyngaa, Torosantucci, Liliana, Torriglia, Alicia, Torrisi, Maria Rosaria, Tournier, Cathy, Towns, Roberto, Trajkovic, Vladimir, Travassos, Leonardo H., Triola, Gemma, Tripathi, Durga Nand, Trisciuoglio, Daniela, Troncoso, Rodrigo, Trougakos, Ioannis P., Truttmann, Anita C., Tsai, Kuen-Jer, Tschan, Mario P., Tseng, Yi-Hsin, Tsukuba, Takayuki, Tsung, Allan, Tsvetkov, Andrey S., Tu, Shuiping, Tuan, Hsing-Yu, Tucci, Marco, Tumbarello, David A., Turk, Bori, Turk, Vito, Turner, Robin F.B., Tveita, Anders A., Tyagi, Suresh C., Ubukata, Makoto, Uchiyama, Yasuo, Udelnow, Andrej, Ueno, Takashi, Umekawa, Midori, Umemiya-Shirafuji, Rika, Underwood, Benjamin R., Ungermann, Christian, Ureshino, Rodrigo P., Ushioda, Ryo, Uversky, Vladimir N., Uzcátegui, Néstor L., Vaccari, Thoma, Vaccaro, Maria I., Váchová, Libuše, Vakifahmetoglu-Norberg, Helin, Valdor, Rut, Valente, Enza Maria, Vallette, Francoi, Valverde, Angela M., Van den Berghe, Greet, Van Den Bosch, Ludo, van den Brink, Gijs R., van der Goot, F. Gisou, van der Klei, Ida J., van der Laan, Luc J.W., van Doorn, Wouter G., van Egmond, Marjolein, van Golen, Kenneth L., Van Kaer, Luc, Campagne, Menno van Lookeren, Vandenabeele, Peter, Vandenberghe, Wim, Vanhorebeek, Ilse, Varela-Nieto, Isabel, Vasconcelos, M. Helena, Vasko, Radovan, Vavvas, Demetrios G., Vega-Naredo, Ignacio, Velasco, Guillermo, Velentzas, Athanassios D., Velentzas, Panagiotis D., Vellai, Tibor, Vellenga, Edo, Vendelbo, Mikkel Holm, Venkatachalam, Kartik, Ventura, Natascia, Ventura, Salvador, Veras, Patrícia S.T., Verdier, Mireille, Vertessy, Beata G., Viale, Andrea, Vidal, Michel, Vieira, Helena L.A., Vierstra, Richard D., Vigneswaran, Nadarajah, Vij, Neeraj, Vila, Miquel, Villar, Margarita, Villar, Victor H., Villarroya, Joan, Vindis, Cécile, Viola, Giampietro, Viscomi, Maria Teresa, Vitale, Giovanni, Vogl, Dan T., Voitsekhovskaja, Olga V., von Haefen, Clarissa, von Schwarzenberg, Karin, Voth, Daniel E., Vouret-Craviari, Valérie, Vuori, Kristina, Vyas, Jatin M., Waeber, Christian, Walker, Cheryl Lyn, Walker, Mark J., Walter, Jochen, Wan, Lei, Wan, Xiangbo, Wang, Bo, Wang, Caihong, Wang, Chao-Yung, Wang, Chengshu, Wang, Chenran, Wang, Chuangui, Wang, Dong, Wang, Fen, Wang, Fuxin, Wang, Guanghui, Wang, Hai-Jie, Wang, Haichao, Wang, Hong-Gang, Wang, Hongmin, Wang, Horng-Dar, Wang, Jing, Wang, Junjun, Wang, Mei, Wang, Mei-Qing, Wang, Pei-Yu, Wang, Peng, Wang, Richard C., Wang, Shuo, Wang, Ting-Fang, Wang, Xian, Wang, Xiao-Jia, Wang, Xiao-Wei, Wang, Xin, Wang, Xuejun, Wang, Yan, Wang, Yanming, Wang, Ying, Wang, Ying-Jan, Wang, Yipeng, Wang, Yu, Wang, Yu Tian, Wang, Yuqing, Wang, Zhi-Nong, Wappner, Pablo, Ward, Carl, Ward, Diane McVey, Warnes, Gary, Watada, Hirotaka, Watanabe, Yoshihisa, Watase, Kei, Weaver, Timothy E., Weekes, Colin D., Wei, Jiwu, Weide, Thoma, Weihl, Conrad C., Weindl, Günther, Weis, Simone Nardin, Wen, Longping, Wen, Xin, Wen, Yunfei, Westermann, Benedikt, Weyand, Cornelia M., White, Anthony R., White, Eileen, Whitton, J. Lindsay, Whitworth, Alexander J., Wiels, Joëlle, Wild, Franziska, Wildenberg, Manon E., Wileman, Tom, Wilkinson, Deepti Sriniva, Wilkinson, Simon, Willbold, Dieter, Williams, Chri, Williams, Katherine, Williamson, Peter R., Winklhofer, Konstanze F., Witkin, Steven S., Wohlgemuth, Stephanie E., Wollert, Thoma, Wolvetang, Ernst J., Wong, Esther, Wong, G. William, Wong, Richard W., Wong, Vincent Kam Wai, Woodcock, Elizabeth A., Wright, Karen L., Wu, Chunlai, Wu, Defeng, Wu, Gen Sheng, Wu, Jian, Wu, Junfang, Wu, Mian, Wu, Min, Wu, Shengzhou, Wu, William K.K., Wu, Yaohua, Wu, Zhenlong, Xavier, Cristina P.R., Xavier, Ramnik J., Xia, Gui-Xian, Xia, Tian, Xia, Weiliang, Xia, Yong, Xiao, Hengyi, Xiao, Jian, Xiao, Shi, Xiao, Wuhan, Xie, Chuan-Ming, Xie, Zhiping, Xie, Zhonglin, Xilouri, Maria, Xiong, Yuyan, Xu, Chuanshan, Xu, Congfeng, Xu, Feng, Xu, Haoxing, Xu, Hongwei, Xu, Jian, Xu, Jianzhen, Xu, Jinxian, Xu, Liang, Xu, Xiaolei, Xu, Yangqing, Xu, Ye, Xu, Zhi-Xiang, Xu, Ziheng, Xue, Yu, Yamada, Takahiro, Yamamoto, Ai, Yamanaka, Koji, Yamashina, Shunhei, Yamashiro, Shigeko, Yan, Bing, Yan, Bo, Yan, Xianghua, Yan, Zhen, Yanagi, Yasuo, Yang, Dun-Sheng, Yang, Jin-Ming, Yang, Liu, Yang, Minghua, Yang, Pei-Ming, Yang, Peixin, Yang, Qian, Yang, Wannian, Yang, Wei Yuan, Yang, Xuesong, Yang, Yi, Yang, Ying, Yang, Zhifen, Yang, Zhihong, Yao, Meng-Chao, Yao, Pamela J., Yao, Xiaofeng, Yao, Zhenyu, Yao, Zhiyuan, Yasui, Linda S., Ye, Mingxiang, Yedvobnick, Barry, Yeganeh, Behzad, Yeh, Elizabeth S., Yeyati, Patricia L., Yi, Fan, Yi, Long, Yin, Xiao-Ming, Yip, Calvin K., Yoo, Yeong-Min, Yoo, Young Hyun, Yoon, Seung-Yong, Yoshida, Ken-Ichi, Yoshimori, Tamotsu, Young, Ken H., Yu, Huixin, Yu, Jane J., Yu, Jin-Tai, Yu, Jun, Yu, Li, Yu, W. Haung, Yu, Xiao-Fang, Yu, Zhengping, Yuan, Junying, Yuan, Zhi-Min, Yue, Beatrice Y.J.T., Yue, Jianbo, Yue, Zhenyu, Zacks, David N., Zacksenhaus, Eldad, Zaffaroni, Nadia, Zaglia, Tania, Zakeri, Zahra, Zecchini, Vincent, Zeng, Jinsheng, Zeng, Min, Zeng, Qi, Zervos, Antonis S., Zhang, Donna D., Zhang, Fan, Zhang, Guo, Zhang, Guo-Chang, Zhang, Hao, Zhang, Hong, Zhang, Hongbing, Zhang, Jian, Zhang, Jiangwei, Zhang, Jianhua, Zhang, Jing-Pu, Zhang, Li, Zhang, Lin, Zhang, Long, Zhang, Ming-Yong, Zhang, Xiangnan, Zhang, Xu Dong, Zhang, Yan, Zhang, Yang, Zhang, Yanjin, Zhang, Yingmei, Zhang, Yunjiao, Zhao, Mei, Zhao, Wei-Li, Zhao, Xiaonan, Zhao, Yan G., Zhao, Ying, Zhao, Yongchao, Zhao, Yu-Xia, Zhao, Zhendong, Zhao, Zhizhuang J., Zheng, Dexian, Zheng, Xi-Long, Zheng, Xiaoxiang, Zhivotovsky, Bori, Zhong, Qing, Zhou, Guang-Zhou, Zhou, Guofei, Zhou, Huiping, Zhou, Shu-Feng, Zhou, Xu-Jie, Zhu, Hongxin, Zhu, Hua, Zhu, Wei-Guo, Zhu, Wenhua, Zhu, Xiao-Feng, Zhu, Yuhua, Zhuang, Shi-Mei, Zhuang, Xiaohong, Ziparo, Elio, Zois, Christos E., Zoladek, Teresa, Zong, Wei-Xing, Zorzano, Antonio, and Zughaier, Susu M.

Subjects
Molecular Biology, Cell Biology, Settore BIO/06 - Anatomia Comparata E Citologia
Abstract

non presente

Published
2016

31. A roadmap for interpreting13C metabolite labeling patterns from cells

Author

Buescher, JM, Antoniewicz, MR, Boros, LG, Burgess, SC, Brunengraber, H, Clish, CB, DeBerardinis, RJ, Feron, O, Frezza, C, Ghesquiere, B, Gottlieb, E, Hiller, K, Jones, RG, Kamphorst, JJ, Kibbey, RG, Kimmelman, AC, Locasale, JW, Lunt, SY, Maddocks, ODK, Malloy, C, Metallo, CM, Meuillet, EJ, Munger, J, Nöh, K, Rabinowitz, JD, Ralser, M, Sauer, U, Stephanopoulos, G, St-Pierre, J, Tennant, DA, Wittmann, C, Vander Heiden, MG, Vazquez, A, Vousden, K, Young, JD, Zamboni, N, and Fendt, SM

Abstract

© 2015 Elsevier Ltd. Measuring intracellular metabolism has increasingly led to important insights in biomedical research.13C tracer analysis, although less information-rich than quantitative13C flux analysis that requires computational data integration, has been established as a time-efficient method to unravel relative pathway activities, qualitative changes in pathway contributions, and nutrient contributions. Here, we review selected key issues in interpreting13C metabolite labeling patterns, with the goal of drawing accurate conclusions from steady state and dynamic stable isotopic tracer experiments.

Published
2015
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32. Designing a broad-spectrum integrative approach for cancer prevention and treatment

Author

Block, KI, Gyllenhaal, C, Lowe, L, Amedei, A, Ruhul Amin, ARM, Amin, A, Aquilano, K, Arbiser, J, Arreola, A, Arzumanyan, A, Salman Ashraf, S, Azmi, AS, Benencia, F, Bhakta, D, Bilsland, A, Bishayee, A, Blain, SW, Block, PB, Boosani, CS, Carey, TE, Carnero, A, Carotenuto, M, Casey, SC, Chakrabarti, M, Chaturvedi, R, Chen, GZ, Chen, H, Chen, S, Chen, YC, Choi, BK, Ciriolo, MR, Coley, HM, Collins, AR, Connell, M, Crawford, S, Curran, CS, Dabrosin, C, Damia, G, Dasgupta, S, DeBerardinis, RJ, Decker, WK, Dhawan, P, Diehl, AME, Dong, JT, Dou, QP, Drewa, JE, Elkord, E, El-Rayes, B, Feitelson, MA, Felsheru, DW, Ferguson, LR, Fimognari, C, Firestone, GL, Frezza, C, Fujii, H, Fuster, MM, Generali, D, Georgakilas, AG, Gieseler, F, Gilbertson, M, Green, MF, Grue, B, Guhal, G, Halicka, D, Helferich, WG, Heneberg, P, Hentosh, P, Hirschey, MD, Hofseth, LJ, Holcombe, RF, Honoki, K, Hsu, HY, Huang, GS, Jensen, LD, Jiang, WG, Jones, LW, Karpowicz, PA, Keith, WN, Kerkar, SP, Khan, GN, Khatami, M, Ko, YH, Kucuk, O, Kulathinal, RJ, Kumar, NB, Kwon, BS, Leb, A, Leab, MA, Lee, HY, Lichtor, T, Lin, LT, and Locasale, JW

Abstract

© 2015 The Authors. Targeted therapies and the consequent adoption of "personalized" oncology have achieved notablesuccesses in some cancers; however, significant problems remain with this approach. Many targetedtherapies are highly toxic, costs are extremely high, and most patients experience relapse after a fewdisease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistantimmortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are notreliant upon the same mechanisms as those which have been targeted). To address these limitations, aninternational task force of 180 scientists was assembled to explore the concept of a low-toxicity "broad-spectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspectsof relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a widerange of high-priority targets (74 in total) that could be modified to improve patient outcomes. For thesetargets, corresponding low-toxicity therapeutic approaches were then suggested, many of which werephytochemicals. Proposed actions on each target and all of the approaches were further reviewed forknown effects on other hallmark areas and the tumor microenvironment. Potential contrary or procar-cinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixedevidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of therelationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. Thisnovel approach has potential to be relatively inexpensive, it should help us address stages and types ofcancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for futureresearch is offered.

Published
2015
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33. Cell surface proteomic map of HIV infection reveals antagonism of amino acid metabolism by Vpu and Nef

Author

Matheson, N.J., Sumner, J., Wals, K., Rapiteanu, R., Weekes, M.P., Vigan, R., Weinelt, J., Schindler, M., Antrobus, R., Costa, A.S.H., Frezza, C., Clish, C.B., Neil, S.J.D., and Lehner, P.J.

Subjects
virus diseases
Abstract

Critical cell surface immunoreceptors downregulated during HIV infection have previously been identified using non-systematic, candidate approaches. To gain a comprehensive, unbiased overview of how HIV infection remodels the T cell surface, we took a distinct, systems-level, quantitative proteomic approach. >100 plasma membrane proteins, many without characterized immune functions, were downregulated during HIV infection. Host factors targeted by the viral accessory proteins Vpu or Nef included the amino acid transporter SNAT1 and the serine carriers SERINC3/5. We focused on SNAT1, a β-TrCP-dependent Vpu substrate. SNAT1 antagonism was acquired by Vpu variants from the lineage of SIVcpz/HIV-1 viruses responsible for pandemic AIDS. We found marked SNAT1 induction in activated primary human CD4+ T cells, and used Consumption and Release (CoRe) metabolomics to identify alanine as an endogenous SNAT1 substrate required for T cell mitogenesis. Downregulation of SNAT1 therefore defines a unique paradigm of HIV interference with immunometabolism.

Published
2015

34. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).

Author

Klionsky, Dj, Abdelmohsen, K, Abe, A, Abedin, Mj, Abeliovich, H, Acevedo Arozena, A, Adachi, H, Adams, Cm, Adams, Pd, Adeli, K, Adhihetty, Pj, Adler, Sg, Agam, G, Agarwal, R, Aghi, Mk, Agnello, M, Agostinis, P, Aguilar, Pv, Aguirre-Ghiso, J, Airoldi, Em, Ait-Si-Ali, S, Akematsu, T, Akporiaye, Et, Al-Rubeai, M, Albaiceta, Gm, Albanese, C, Albani, D, Albert, Ml, Aldudo, J, Algül, H, Alirezaei, M, Alloza, I, Almasan, A, Almonte-Beceril, M, Alnemri, E, Alonso, C, Altan-Bonnet, N, Altieri, Dc, Alvarez, S, Alvarez-Erviti, L, Alves, S, Amadoro, G, Amano, A, Amantini, C, Ambrosio, S, Amelio, I, Amer, Ao, Amessou, M, Amon, A, An, Z, Anania, Fa, Andersen, Su, Andley, Up, Andreadi, Ck, Andrieu-Abadie, N, Anel, A, Ann, Dk, Anoopkumar-Dukie, S, Antonioli, M, Aoki, H, Apostolova, N, Aquila, S, Aquilano, K, Araki, K, Arama, E, Aranda, A, Araya, J, Arcaro, A, Arias, E, Arimoto, H, Ariosa, Ar, Armstrong, Jl, Arnould, T, Arsov, I, Asanuma, K, Askanas, V, Asselin, E, Atarashi, R, Atherton, S, Atkin, Jd, 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Starokadomskyy, P, Steegborn, C, Steele, Jw, Stefanis, L, Steffan, J, Stellrecht, Cm, Stenmark, H, Stepkowski, Tm, Stern, St, Stevens, C, Stockwell, Br, Stoka, V, Storchova, Z, Stork, B, Stratoulias, V, Stravopodis, Dj, Strnad, P, Strohecker, Am, Ström, Al, Stromhaug, P, Stulik, J, Su, Yx, Su, Z, Subauste, C, Subramaniam, S, Sue, Cm, Suh, Sw, Sui, X, Sukseree, S, Sulzer, D, Sun, Fl, Sun, J, Sun, Sy, Sun, Y, Sundaramoorthy, V, Sung, J, Suzuki, H, Suzuki, K, Suzuki, N, Suzuki, T, Suzuki, Yj, Swanson, M, Swanton, C, Swärd, K, Swarup, G, Sweeney, St, Sylvester, Pw, Szatmari, Z, Szegezdi, E, Szlosarek, Pw, Taegtmeyer, H, Tafani, M, Taillebourg, E, Tait, Sw, Takacs-Vellai, K, Takahashi, Y, Takáts, S, Takemura, G, Takigawa, N, Talbot, Nj, Tamagno, E, Tamburini, J, Tan, Cp, Tan, L, Tan, Ml, Tan, M, Tan, Yj, Tanaka, K, Tanaka, M, Tang, D, Tang, G, Tanida, I, Tanji, K, Tannous, Ba, Tapia, Ja, Tasset-Cuevas, I, Tatar, M, Tavassoly, I, Tavernarakis, N, Taylor, A, Taylor, G, Taylor, Ga, Taylor, Jp, Taylor, Mj, Tchetina, Ev, Tee, Ar, Teixeira-Clerc, F, Telang, S, Tencomnao, T, Teng, Bb, Teng, Rj, Terro, F, Tettamanti, G, Theiss, Al, Theron, Ae, Thomas, Kj, Thomé, Mp, Thomes, Pg, Thorburn, A, Thorner, J, Thum, T, Thumm, M, Thurston, Tl, Tian, L, Till, A, Ting, Jp, Titorenko, Vi, Toker, L, Toldo, S, Tooze, Sa, Topisirovic, I, Torgersen, Ml, Torosantucci, L, Torriglia, A, Torrisi, Mr, Tournier, C, Towns, R, Trajkovic, V, Travassos, Lh, Triola, G, Tripathi, Dn, Trisciuoglio, D, Troncoso, R, Trougakos, Ip, Truttmann, Ac, Tsai, Kj, Tschan, Mp, Tseng, Yh, Tsukuba, T, Tsung, A, Tsvetkov, A, Tu, S, Tuan, Hy, Tucci, M, Tumbarello, Da, Turk, B, Turk, V, Turner, Rf, Tveita, Aa, Tyagi, Sc, Ubukata, M, Uchiyama, Y, Udelnow, A, Ueno, T, Umekawa, M, Umemiya-Shirafuji, R, Underwood, Br, Ungermann, C, Ureshino, Rp, Ushioda, R, Uversky, Vn, Uzcátegui, Nl, Vaccari, T, Vaccaro, Mi, Váchová, L, Vakifahmetoglu-Norberg, H, Valdor, R, Valente, Em, Vallette, F, Valverde, Am, Van den Berghe, G, Van Den Bosch, L, van den Brink, Gr, van der Goot, Fg, van der Klei, Ij, van der Laan, Lj, van Doorn, Wg, van Egmond, M, van Golen, Kl, Van Kaer, L, van Lookeren Campagne, M, Vandenabeele, P, Vandenberghe, W, Vanhorebeek, I, Varela-Nieto, I, Vasconcelos, Mh, Vasko, R, Vavvas, Dg, Vega-Naredo, I, Velasco, G, Velentzas, Ad, Velentzas, Pd, Vellai, T, Vellenga, E, Vendelbo, Mh, Venkatachalam, K, Ventura, N, Ventura, S, Veras, P, Verdier, M, Vertessy, Bg, Viale, A, Vidal, M, Vieira, Hl, Vierstra, Rd, Vigneswaran, N, Vij, N, Vila, M, Villar, M, Villar, Vh, Villarroya, J, Vindis, C, Viola, G, Viscomi, Maria Teresa, Vitale, G, Vogl, Dt, Voitsekhovskaja, Ov, von Haefen, C, von Schwarzenberg, K, Voth, De, Vouret-Craviari, V, Vuori, K, Vyas, Jm, Waeber, C, Walker, Cl, Walker, Mj, Walter, J, Wan, L, Wan, X, Wang, B, Wang, C, Wang, Cy, Wang, D, Wang, F, Wang, G, Wang, Hj, Wang, H, Wang, Hg, Wang, Hd, Wang, J, Wang, M, Wang, Mq, Wang, Py, Wang, P, Wang, Rc, Wang, S, Wang, Tf, Wang, X, Wang, Xj, Wang, Xw, 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Abstract

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we prese

Published
2016

35. Inflammation and programmed cell death in Alzheimer's disease: comparison of the central nervous system and peripheral blood

Author

Macchi B.(1), Marino-Merlo F. (2), Frezza C. (3), Cuzzocrea S. (2, and Mastino A (2

Subjects
Central Nervous System, Programmed cell death, medicine.medical_specialty, Neurology, Central nervous system, Neuroscience (miscellaneous), Apoptosis, Inflammation, Disease, Cellular and Molecular Neuroscience, Alzheimer Disease, medicine, Animals, Humans, Cell damage, Caspase, Alzheimer, CNS, Peripheral blood, Inflammation, Apoptosis, caspases, NF-kB, Neurodegenerations, Alzheimer, PBMC, biology, Neurodegeneration, Settore BIO/14, medicine.disease, Oxidative Stress, medicine.anatomical_structure, Immunology, Disease Progression, biology.protein, medicine.symptom, Neuroscience
Abstract

Although the central nervous system (CNS) has been defined as a privileged site in Alzheimer's disease (AD), periphery can be more than simply witness of events leading to neurodegeneration. The CNS and peripheral blood can mutually communicate through cells and factors trafficking from the circulation into the brain and vice versa. A number of articles have reviewed inflammatory profiles and programmed cell death (PCD) in AD, separately in the CNS and at the peripheral level. This review does not provide an exhaustive account of what has been published on inflammation and PCD in AD. Rather, the aim of this review is to focus on possible linkages between the central and the peripheral compartments during AD progression, by critically analyzing, in a comparative manner, phenomena occurring in the CNS as well as the peripheral blood. In fact, growing evidence suggests that CNS and peripheral inflammation might present common features in the disease. Microarrays and metabolomics revealed that dysfunction of the glycolytic and oxidative pathways is similar in the brain and in the periphery. Moreover, dysregulated autophagosome/lysosomal molecular machinery, both at the CNS and the peripheral level, in AD-related cell damage, has been observed. Possible implications of these observations have been discussed.

Published
2014
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37. Phytochemistry, micromorphology and bioactivities of Ajuga chamaepitys (L.) Schreb. (Lamiaceae, Ajugoideae): Two new harpagide derivatives and an unusual iridoid glycosides pattern

Author

Venditti, A., primary, Frezza, C., additional, Maggi, F., additional, Lupidi, G., additional, Bramucci, M., additional, Quassinti, L., additional, Giuliani, C., additional, Cianfaglione, K., additional, Papa, F., additional, Serafini, M., additional, and Bianco, A., additional

Published
2016
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40. A novel, cell-free PCR-based assay for evaluating the inhibitory activity of antiretroviral compounds against HIV reverse transcriptase

Author

Frezza, C., Balestrieri, E., MARINO MERLO, Francesca, Mastino, Antonio, and Macchi, B.

Subjects
Cyclopropanes, DNA, Complementary, Anti-HIV Agents, antiviral drug resistance, Settore BIO/14, Drug Evaluation, Preclinical, Reproducibility of Results, Microbial Sensitivity Tests, Reverse Transcription, antiviral agents, HIV-1 reverse transcriptase, non-nucleoside reverse transcriptase inhibitor, Settore MED/07 - Microbiologia e Microbiologia Clinica, Polymerase Chain Reaction, Sensitivity and Specificity, HIV Reverse Transcriptase, Benzoxazines, Alkynes, Humans, Reverse Transcriptase Inhibitors, Nevirapine
Abstract

This study describes a novel, PCR-based assay that evaluates the ability of compounds to inhibit cDNA generation by HIV reverse transcriptase (RT), of both commercial and viral lysate origin, from a known RNA template. The template consisted of RNA from stable transfectants ectopically expressing the US6 gene of herpes simplex virus-1, coding for glycoprotein D. Controls were carried out to demonstrate that no residual DNA polymerase activity or DNA contamination was responsible for the amplified DNA in the tested, control samples. In this assay, 0.1 μM nevirapine totally inhibited the RT activity of 0.5 U commercial HIV RT, while 10 nM inhibited it by only 10%. Conversely, 10 pM efavirenz completely inhibited 0.5 U HIV RT. Similar results were obtained when a self-prepared viral lysate was used as a source of HIV RT. A reference commercial kit directly measuring HIV RT activity, without amplification, was less sensitive than the new assay. As a consequence, the HIV RT 50% inhibitory concentration of nevirapine and efavirenz in the newly described assay was 8 and 5 × 10(3) times lower, respectively, than in the commercial assay. In conclusion, this novel method was sensitive, reproducible, and sufficiently rapid for screening in vitro the functional activity of known or potential antiretroviral compounds against HIV RT.

Published
2013

41. Succinate is a danger signal that induces IL-1β via HIF-1α

Author

Tannahill, GM, Curtis, AM, Adamik, J, Palsson-McDermott, EM, McGettrick, AF, Goel, G, Frezza, C, Bernard, NJ, Kelly, B, Foley, NH, Zheng, L, Gardet, A, Tong, Z, Jany, SS, Corr, SC, Haneklaus, M, Caffery, BE, Pierce, K, Walmsley, S, Beasley, FC, Cummins, E, Nizet, V, Whyte, M, Taylor, CT, Lin, H, Masters, SL, Gottlieb, E, Kelly, VP, Clish, C, Auron, PE, Xavier, RJ, and O’Neill, LAJ

Subjects
Male, Immunity, Humans, Communicable Diseases, Article
Abstract

Macrophages activated by the gram negative bacterial product lipopolysaccharide (LPS) switch their core metabolism from oxidative phosphorylation to glycolysis1. Inhibition of glycolysis with 2-deoxyglucose (2DG) suppressed LPS-induced Interleukin-1 beta (IL-1β) but not Tumour necrosis factor alpha (TNFα) in macrophages. A comprehensive metabolic map of LPS-activated macrophages revealed up-regulation of glycolytic and down-regulation of mitochondrial genes, which correlated directly with the expression profiles of altered metabolites. LPS strongly increased the TCA cycle intermediate succinate. Glutamine-dependent anerplerosis was the major source of succinate with the ‘Gamma-Aminobutyric Acid (GABA)-shunt’ pathway also playing a role. LPS-induced succinate stabilized Hypoxia-inducible factor 1α (HIF-1α), an effect inhibited by 2DG, with IL-1β as an important target. LPS also increases succinylation of several proteins. Succinate is therefore identified as a metabolite in innate immune signalling which leads to enhanced IL-1β production during inflammation.

Published
2013

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