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3. A white paper from the FEBS Education and Training Conference: challenges, opportunities, and action plans for transforming molecular life sciences education.

Author

Villo, Ly, Sincic, Nino, Mello, Luciane V., Costa, Manuel Joao, Picard, Didier, Malatesta, Francesco, Dumic, Jerka, and Sagin, Ferhan G.

Subjects
EDUCATION conferences, LIFE science education, TECHNOLOGICAL innovations, SCIENCE conferences, DIGITAL technology
Abstract

The inaugural FEBS Education and Training Conference (ETC) was held in Türkiye, in 2024. This first‐ever Molecular Life Sciences Education Conference in Europe was organized by the FEBS Education and Training Committee and it was a groundbreaking event that brought together educators and scientists to explore how to enhance education and training in molecular life sciences. The conference explored a wide range of critical themes, for example—digital revolution, active learning and student engagement, multidisciplinary teaching and learning, transitions and inclusivity in education, students' self‐assessment, and self‐regulated learning. The discussions and presentations underscored the pressing need for transformation in how academics and researchers approach teaching and learning. Such shift is driven by rapid technological advancements, societal shifts, and the evolving demands of the scientific landscape. This document synthesizes key insights, discussions, and recommendations from the conference and proposes actionable strategies for all stakeholders in the field—institutions, educators and students—to address current challenges in education and training in molecular life sciences. [ABSTRACT FROM AUTHOR]

Published
2025
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8. Dynamic Imaging of LDH Inhibition in Tumors Reveals Rapid In Vivo Metabolic Rewiring and Vulnerability to Combination Therapy

Author

Oshima, Nobu, Ishida, Ryo, Kishimoto, Shun, Beebe, Kristin, Brender, Jeffrey R., Yamamoto, Kazutoshi, Urban, Daniel, Rai, Ganesha, Johnson, Michelle S., Benavides, Gloria, Squadrito, Giuseppe L., Crooks, Dan, Jackson, Joseph, Joshi, Abhinav, Mott, Bryan T., Shrimp, Jonathan H., Moses, Michael A., Lee, Min-Jung, Yuno, Akira, Lee, Tobie D., Hu, Xin, Anderson, Tamara, Kusewitt, Donna, Hathaway, Helen H., Jadhav, Ajit, Picard, Didier, Trepel, Jane B., Mitchell, James B., Stott, Gordon M., Moore, William, Simeonov, Anton, Sklar, Larry A., Norenberg, Jeffrey P., Linehan, W. Marston, Maloney, David J., Dang, Chi V., Waterson, Alex G., Hall, Matthew, Darley-Usmar, Victor M., Krishna, Murali C., and Neckers, Leonard M.

Published
2020
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14. Molecular chaperone TRAP1 regulates a metabolic switch between mitochondrial respiration and aerobic glycolysis.

Author

Yoshida, Soichiro, Tsutsumi, Shinji, Muhlebach, Guillaume, Sourbier, Carole, Lee, Min-Jung, Lee, Sunmin, Vartholomaiou, Evangelia, Tatokoro, Manabu, Beebe, Kristin, Miyajima, Naoto, Mohney, Robert, Chen, Yang, Hasumi, Hisashi, Xu, Wanping, Fukushima, Hiroshi, Koga, Fumitaka, Kihara, Kazunori, Trepel, Jane, Picard, Didier, Neckers, Leonard, and Nakamura, Ken

Subjects
Animals, COS Cells, CSK Tyrosine-Protein Kinase, Chlorocebus aethiops, Glycolysis, HSP90 Heat-Shock Proteins, HeLa Cells, Humans, Intracellular Signaling Peptides and Proteins, Mice, Mice, Knockout, Mitochondria, Mitochondrial Proteins, Molecular Chaperones, NIH 3T3 Cells, Neoplasm Invasiveness, Oxidative Phosphorylation, RNA Interference, Transfection, src-Family Kinases
Abstract

TRAP1 (TNF receptor-associated protein), a member of the HSP90 chaperone family, is found predominantly in mitochondria. TRAP1 is broadly considered to be an anticancer molecular target. However, current inhibitors cannot distinguish between HSP90 and TRAP1, making their utility as probes of TRAP1-specific function questionable. Some cancers express less TRAP1 than do their normal tissue counterparts, suggesting that TRAP1 function in mitochondria of normal and transformed cells is more complex than previously appreciated. We have used TRAP1-null cells and transient TRAP1 silencing/overexpression to show that TRAP1 regulates a metabolic switch between oxidative phosphorylation and aerobic glycolysis in immortalized mouse fibroblasts and in human tumor cells. TRAP1-deficiency promotes an increase in mitochondrial respiration and fatty acid oxidation, and in cellular accumulation of tricarboxylic acid cycle intermediates, ATP and reactive oxygen species. At the same time, glucose metabolism is suppressed. TRAP1-deficient cells also display strikingly enhanced invasiveness. TRAP1 interaction with and regulation of mitochondrial c-Src provide a mechanistic basis for these phenotypes. Taken together with the observation that TRAP1 expression is inversely correlated with tumor grade in several cancers, these data suggest that, in some settings, this mitochondrial molecular chaperone may act as a tumor suppressor.

Published
2013

26. Metformin reverses TRAP1 mutation-associated alterations in mitochondrial function in Parkinsonʼs disease

Author

Fitzgerald, Julia C., Zimprich, Alexander, Carvajal Berrio, Daniel A., Schindler, Kevin M., Maurer, Brigitte, Schulte, Claudia, Bus, Christine, Hauser, Anne-Kathrin, Kübler, Manuela, Lewin, Rahel, Bobbili, Dheeraj Reddy, Schwarz, Lisa M., Vartholomaiou, Evangelia, Brockmann, Kathrin, Wüst, Richard, Madlung, Johannes, Nordheim, Alfred, Riess, Olaf, Martins, Miguel L., Glaab, Enrico, May, Patrick, Schenke-Layland, Katja, Picard, Didier, Sharma, Manu, Gasser, Thomas, and Krüger, Rejko

Published
2017
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47. H90-10 single-chain antibody recognizes Hsp90beta by immunoprecipitation and Western blotting

Author

Abboud, Ernest, Bernasconi, Lilia, and Picard, Didier

Subjects
biology, Chemistry, Immunoprecipitation, Immunoblotting, Hsp90, Endogeny, General Medicine, Single chain, Molecular biology, law.invention, Blot, law, ddc:570, Molecular chaperone, biology.protein, Recombinant DNA, Antibody, Beta (finance)
Abstract

The recombinant antibody H90-10 detects the endogenous human heat-shock protein 90 beta (Hsp90β) by immunoprecipitation (IP) and Western blotting.

Published
2021
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50. Genetic Ablation of MiR-22 Fosters Diet-Induced Obesity and NAFLD Development

Author

Gjorgjieva, Monika, Sobolewski, Cyril, Ay, Anne-Sophie, Abegg, Daniel, Sousa, Marta Correia de, Portius, Dorothea, Berthou, Flavien, Fournier, Margot, Maeder, Christine, Rantakari, Pia, Zhang, Fu-Ping, Poutanen, Matti, Picard, Didier, Montet, Xavier, Nef, Serge, Adibekian, Alexander, and Foti, Michelangelo

Subjects
obesity, ddc:570, lcsh:R, lipid metabolism, lcsh:Medicine, fatty liver disease, ddc:576.5, glycolysis, ddc:612, ddc:616.0757, Article, microRNAs
Abstract

miR-22 is one of the most abundant miRNAs in the liver and alterations of its hepatic expression have been associated with the development of hepatic steatosis and insulin resistance, as well as cancer. However, the pathophysiological roles of miR-22-3p in the deregulated hepatic metabolism with obesity and cancer remains poorly characterized. Herein, we observed that alterations of hepatic miR-22-3p expression with non-alcoholic fatty liver disease (NAFLD) in the context of obesity are not consistent in various human cohorts and animal models in contrast to the well-characterized miR-22-3p downregulation observed in hepatic cancers. To unravel the role of miR-22 in obesity-associated NAFLD, we generated constitutive Mir22 knockout (miR-22KO) mice, which were subsequently rendered obese by feeding with fat-enriched diet. Functional NAFLD- and obesity-associated metabolic parameters were then analyzed. Insights about the role of miR-22 in NAFLD associated with obesity were further obtained through an unbiased proteomic analysis of miR-22KO livers from obese mice. Metabolic processes governed by miR-22 were finally investigated in hepatic transformed cancer cells. Deletion of Mir22 was asymptomatic when mice were bred under standard conditions, except for an onset of glucose intolerance. However, when challenged with a high fat-containing diet, Mir22 deficiency dramatically exacerbated fat mass gain, hepatomegaly, and liver steatosis in mice. Analyses of explanted white adipose tissue revealed increased lipid synthesis, whereas mass spectrometry analysis of the liver proteome indicated that Mir22 deletion promotes hepatic upregulation of key enzymes in glycolysis and lipid uptake. Surprisingly, expression of miR-22-3p in Huh7 hepatic cancer cells triggers, in contrast to our in vivo observations, a clear induction of a Warburg effect with an increased glycolysis and an inhibited mitochondrial respiration. Together, our study indicates that miR-22-3p is a master regulator of the lipid and glucose metabolism with differential effects in specific organs and in transformed hepatic cancer cells, as compared to non-tumoral tissue.

Published
2020

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