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1. Hippo-YAP/TAZ signalling coordinates adipose plasticity and energy balance by uncoupling leptin expression from fat mass.

Author

Choi, Sungwoo, Kang, Ju-Gyeong, Tran, Yen, Jeong, Sun-Hye, Park, Kun-Young, Shin, Hyemi, Kim, Young, Park, Myungsun, Nahmgoong, Hahn, Seol, Taejun, Jeon, Haeyon, Kim, Yeongmin, Park, Sanghee, Kim, Hee-Joo, Kim, Min-Seob, Li, Xiaoxu, Bou Sleiman, Maroun, Lee, Eries, Choi, Jinhyuk, Eisenbarth, David, Lee, Sang, Cho, Suhyeon, Auwerx, Johan, Kim, Il-Young, Kim, Jae, Park, Jong-Eun, Lim, Dae-Sik, Suh, Jae, and Moore, David

Subjects
Animals, Leptin, Signal Transduction, Energy Metabolism, Protein Serine-Threonine Kinases, Mice, Adaptor Proteins, Signal Transducing, YAP-Signaling Proteins, Adipose Tissue, Adipocytes, Hippo Signaling Pathway, Cell Cycle Proteins, Transcription Factors, Transcriptional Coactivator with PDZ-Binding Motif Proteins, Phosphoproteins, Tumor Suppressor Proteins, Trans-Activators
Abstract

Adipose tissues serve as an energy reservoir and endocrine organ, yet the mechanisms that coordinate these functions remain elusive. Here, we show that the transcriptional coregulators, YAP and TAZ, uncouple fat mass from leptin levels and regulate adipocyte plasticity to maintain metabolic homeostasis. Activating YAP/TAZ signalling in adipocytes by deletion of the upstream regulators Lats1 and Lats2 results in a profound reduction in fat mass by converting mature adipocytes into delipidated progenitor-like cells, but does not cause lipodystrophy-related metabolic dysfunction, due to a paradoxical increase in circulating leptin levels. Mechanistically, we demonstrate that YAP/TAZ-TEAD signalling upregulates leptin expression by directly binding to an upstream enhancer site of the leptin gene. We further show that YAP/TAZ activity is associated with, and functionally required for, leptin regulation during fasting and refeeding. These results suggest that adipocyte Hippo-YAP/TAZ signalling constitutes a nexus for coordinating adipose tissue lipid storage capacity and systemic energy balance through the regulation of adipocyte plasticity and leptin gene transcription.

Published
2024

2. Targeting senescence induced by age or chemotherapy with a polyphenol-rich natural extract improves longevity and healthspan in mice

Author

Zumerle, Sara, Sarill, Miles, Saponaro, Miriam, Colucci, Manuel, Contu, Liliana, Lazzarini, Edoardo, Sartori, Roberta, Pezzini, Camilla, Rinaldi, Anna, Scanu, Anna, Sgrignani, Jacopo, Locatelli, Patrizia, Sabbadin, Marianna, Valdata, Aurora, Brina, Daniela, Giacomini, Isabella, Rizzo, Beatrice, Pierantoni, Alessandra, Sharifi, Saman, Bressan, Silvia, Altomare, Claudia, Goshovska, Yulia, Giraudo, Chiara, Luisetto, Roberto, Iaccarino, Luca, Torcasio, Cristina, Mosole, Simone, Pasquini, Emiliano, Rinaldi, Andrea, Pellegrini, Laura, Peron, Gregorio, Fassan, Matteo, Masiero, Stefano, Giori, Andrea Maria, Dall’Acqua, Stefano, Auwerx, Johan, Cippà, Pietro, Cavalli, Andrea, Bolis, Marco, Sandri, Marco, Barile, Lucio, Montopoli, Monica, and Alimonti, Andrea

Published
2024
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4. Data integration in systems genetics and aging research

Author

Rapin, Alexis, Sleiman, Maroun Bou, and Auwerx, Johan

Subjects
Quantitative Biology - Other Quantitative Biology
Abstract

Human life expectancy has dramatically improved over the course of the last century. Although this reflects a global improvement in sanitation and medical care, this also implies that more people suffer from diseases that typically manifest later in life, like Alzheimer and atherosclerosis. Increasing healthspan by delaying or reverting the development of these age-related diseases has therefore become an urgent challenge in biomedical research. Research in this field is complicated by the multi-factorial nature of age-related diseases. They are rooted in complex physiological mechanisms impacted by heritable, environment and life-style factors that can be unique to each individual. Although technological advances in high-throughput biomolecular assays have enabled researchers to investigate individual physiology at the molecular level, integrating information about its different components, and accounting for individual variations remains a challenge. We are using a large collection of omics and phenotype data derived from the BXD mouse genetic diversity panel to explore how good data management practices, as fostered by the FAIR principles, paired with an explainable artificial intelligence framework, can provide solutions to decipher the complex roots of age-related diseases. These developments will help to propose innovative approaches to extend healthspan in the aging global population., Comment: 7 pages, 3 figures, Proceedings of the Swiss Research Data Day 2020, Oct. 22 2020. For full conference proceedings see http://www.ressi.ch/sites/default/files/No_special_DLCM.pdf

Published
2022

13. Embracing cancer complexity: Hallmarks of systemic disease

Author

Swanton, Charles, Bernard, Elsa, Abbosh, Chris, André, Fabrice, Auwerx, Johan, Balmain, Allan, Bar-Sagi, Dafna, Bernards, René, Bullman, Susan, DeGregori, James, Elliott, Catherine, Erez, Ayelet, Evan, Gerard, Febbraio, Mark A., Hidalgo, Andrés, Jamal-Hanjani, Mariam, Joyce, Johanna A., Kaiser, Matthew, Lamia, Katja, Locasale, Jason W., Loi, Sherene, Malanchi, Ilaria, Merad, Miriam, Musgrave, Kathryn, Patel, Ketan J., Quezada, Sergio, Wargo, Jennifer A., Weeraratna, Ashani, White, Eileen, Winkler, Frank, Wood, John N., Vousden, Karen H., and Hanahan, Douglas

Published
2024
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14. Inhibition of SIRT7 overcomes sorafenib acquired resistance by suppressing ERK1/2 phosphorylation via the DDX3X-mediated NLRP3 inflammasome in hepatocellular carcinoma

Author

Kim, Yuna, Jung, Kwan-Young, Kim, Yun Hak, Xu, Pan, Kang, Baeki E., Jo, Yunju, Pandit, Navin, Kwon, Jeongho, Gariani, Karim, Gariani, Joanna, Lee, Junguee, Verbeek, Jef, Nam, Seungyoon, Bae, Sung-Jin, Ha, Ki-Tae, Yi, Hyon-Seung, Shong, Minho, Kim, Kyun-Hwan, Kim, Doyoun, Jung, Hee Jung, Lee, Chang-Woo, Kim, Kwang Rok, Schoonjans, Kristina, Auwerx, Johan, and Ryu, Dongryeol

Published
2024
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16. Mitochondrial matrix protein LETMD1 maintains thermogenic capacity of brown adipose tissue in male mice

Author

Park, Anna, Kim, Kwang-eun, Park, Isaac, Lee, Sang Heon, Park, Kun-Young, Jung, Minkyo, Li, Xiaoxu, Sleiman, Maroun Bou, Lee, Su Jeong, Kim, Dae-Soo, Kim, Jaehoon, Lim, Dae-Sik, Woo, Eui-Jeon, Lee, Eun Woo, Han, Baek Soo, Oh, Kyoung-Jin, Lee, Sang Chul, Auwerx, Johan, Mun, Ji Young, Rhee, Hyun-Woo, Kim, Won Kon, Bae, Kwang-Hee, and Suh, Jae Myoung

Published
2023
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19. Eosinophils regulate adipose tissue inflammation and sustain physical and immunological fitness in old age

Author

Brigger, Daniel, Riether, Carsten, van Brummelen, Robin, Mosher, Kira I, Shiu, Alicia, Ding, Zhaoqing, Zbären, Noemi, Gasser, Pascal, Guntern, Pascal, Yousef, Hanadie, Castellano, Joseph M, Storni, Federico, Graff-Radford, Neill, Britschgi, Markus, Grandgirard, Denis, Hinterbrandner, Magdalena, Siegrist, Mark, Moullan, Norman, Hofstetter, Willy, Leib, Stephen L, Villiger, Peter M, Auwerx, Johan, Villeda, Saul A, Wyss-Coray, Tony, Noti, Mario, and Eggel, Alexander

Subjects
Biomedical and Clinical Sciences, Immunology, Obesity, Aging, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Adipose Tissue, Adipose Tissue, White, Adult, Aged, Animals, Eosinophils, Gene Expression Regulation, Glucose Tolerance Test, Homeostasis, Humans, Immunity, Inflammation, Interleukin-4, Mice, Mice, Inbred C57BL, Middle Aged, Muscle Strength, Physical Fitness, Satellite Cells, Skeletal Muscle, Young Adult, Medical biochemistry and metabolomics, Medical physiology, Nutrition and dietetics
Abstract

Adipose tissue eosinophils (ATEs) are important in the control of obesity-associated inflammation and metabolic disease. However, the way in which ageing impacts the regulatory role of ATEs remains unknown. Here, we show that ATEs undergo major age-related changes in distribution and function associated with impaired adipose tissue homeostasis and systemic low-grade inflammation in both humans and mice. We find that exposure to a young systemic environment partially restores ATE distribution in aged parabionts and reduces adipose tissue inflammation. Approaches to restore ATE distribution using adoptive transfer of eosinophils from young mice into aged recipients proved sufficient to dampen age-related local and systemic low-grade inflammation. Importantly, restoration of a youthful systemic milieu by means of eosinophil transfers resulted in systemic rejuvenation of the aged host, manifesting in improved physical and immune fitness that was partially mediated by eosinophil-derived IL-4. Together, these findings support a critical function of adipose tissue as a source of pro-ageing factors and uncover a new role of eosinophils in promoting healthy ageing by sustaining adipose tissue homeostasis.

Published
2020

20. Sphingolipids accumulate in aged muscle, and their reduction counteracts sarcopenia

Author

Laurila, Pirkka-Pekka, Wohlwend, Martin, Imamura de Lima, Tanes, Luan, Peiling, Herzig, Sébastien, Zanou, Nadège, Crisol, Barbara, Bou-Sleiman, Maroun, Porcu, Eleonora, Gallart-Ayala, Hector, Handzlik, Michal K., Wang, Qi, Jain, Suresh, D’Amico, Davide, Salonen, Minna, Metallo, Christian M., Kutalik, Zoltan, Eichmann, Thomas O., Place, Nicolas, Ivanisevic, Julijana, Lahti, Jari, Eriksson, Johan G., and Auwerx, Johan

Published
2022
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24. NCoR1 Protects Mice From Dextran Sodium Sulfate–Induced Colitis by Guarding Colonic Crypt Cells From Luminal Insult

Author

Mennillo, Elvira, Yang, Xiaojing, Paszek, Miles, Auwerx, Johan, Benner, Christopher, and Chen, Shujuan

Subjects
Medical Biotechnology, Biological Sciences, Biomedical and Clinical Sciences, Digestive Diseases, Stem Cell Research - Nonembryonic - Non-Human, Inflammatory Bowel Disease, Genetics, Human Genome, Stem Cell Research, Autoimmune Disease, Cancer, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Acetylation, Adult Stem Cells, Animals, Apoptosis, Butyrates, Cell Proliferation, Colitis, Ulcerative, Colon, Dextran Sulfate, Disease Models, Animal, Epigenesis, Genetic, Epithelial Cells, Female, Histones, Humans, Intestinal Mucosa, Male, Mice, Mice, Transgenic, Nuclear Receptor Co-Repressor 1, Organoids, Primary Cell Culture, NCoR1, Ulcerative Colitis, Colonic Crypt Cell, Butyrate, Biochemistry and cell biology, Clinical sciences
Abstract

Background & aimsColonic stem cells are essential for producing the mucosal lining, which in turn protects stem cells from insult by luminal factors. Discovery of genetic and biochemical events that control stem cell proliferation and differentiation can be leveraged to decipher the causal factors of ulcerative colitis and aid the development of more effective therapy.MethodsWe performed in vivo and in vitro studies from control (nuclear receptor corepressor 1 [NCoR1F/F]) and intestinal epithelial cell-specific NCoR1-deficient mice (NCoR1ΔIEC). Mice were challenged with dextran sodium sulfate to induce experimental ulcerative colitis, followed by colitis examination, barrier permeability analysis, cell proliferation immunostaining assays, and RNA sequencing analysis. By using crypt cultures, the organoid-forming efficiency, cell proliferation, apoptosis, and histone acetylation were analyzed after butyrate and/or tumor necrosis factor α treatments.ResultsNCoR1ΔIEC mice showed a dramatic increase in disease severity in this colitis model, with suppression of proliferative cells at the crypt base as an early event and a concomitant increase in barrier permeability. Genome expression patterns showed an important role for NCoR1 in colonic stem cell proliferation and secretory cell differentiation. Colonic organoids cultured from NCoR1ΔIEC mice were more sensitive to butyrate-induced cell growth inhibition and apoptosis, which were exaggerated further by tumor necrosis factor α co-treatment, which was accompanied by increased histone acetylation.ConclusionsNCoR1 regulates colonic stem cell proliferation and secretory cell differentiation. When NCoR1 is disrupted, barrier protection is weakened, allowing luminal products such as butyrate to penetrate and synergistically damage the colonic crypt cells. Transcript profiling: RNA sequencing data have been deposited in the GEO database, accession number: GSE136153.

Published
2020

25. Integrative systems analysis identifies genetic and dietary modulators of bile acid homeostasis

Author

Li, Hao, Perino, Alessia, Huang, Qingyao, Von Alvensleben, Giacomo V.G., Banaei-Esfahani, Amir, Velazquez-Villegas, Laura A., Gariani, Karim, Korbelius, Melanie, Bou Sleiman, Maroun, Imbach, Jéromine, Sun, Yu, Li, Xiaoxu, Bachmann, Alexis, Goeminne, Ludger J.E., Gallart-Ayala, Hector, Williams, Evan G., Ivanisevic, Julijana, Auwerx, Johan, and Schoonjans, Kristina

Published
2022
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27. Increased hepatic PDGF-AA signaling mediates liver insulin resistance in obesity associated type 2 diabetes

Author

Abderrahmani, Amar, Yengo, Loic, Caiazzo, Robert, Canouil, Mickael, Cauchi, Stephane, Raverdy, Violeta, Plaisance, Valerie, Pawlowski, Valerie, Lobbens, Stephane, Maillet, Julie, Rolland, Laure, Boutry, Raphael, Queniat, Gurvan, Kwapich, Maxime, Tenenbaum, Mathie, Bricambert, Julien, Saussenthaler, Sophie, Anthony, Elodie, Jha, Pooja, Derop, Julien, Sand, Olivier, Rabearivelo, Iandry, Leloire, Audrey, Pigeyre, Marie, Daujat-Chavanieu, Martine, Gerbal-Chaloin, Sabine, Dayeh, Tasnim, Lassailly, Guillaume, Mathurin, Philippe, Staels, Bart, Auwerx, Johan, Schurmann, Annette, Postic, Catherine, Schafmayer, Clemens, Hampe, Jochen, Bonnefond, Amelie, Pattou, Francois, and Froguel, Philippe

Subjects
Quantitative Biology - Cell Behavior
Abstract

Type 2 diabetes (T2D) is closely linked with non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance, but the involved mechanisms are still elusive. Using DNA methylome and transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in PDGFA (encoding platelet derived growth factor alpha) and PDGFA overexpression are associated with increased T2D risk, hyperinsulinemia, increased insulin resistance and increased steatohepatitis risk. Both genetic risk score studies and human cell modeling pointed to a causative impact of high insulin levels on PDGFA CpG site hypomethylation, PDGFA overexpression, and increased PDGF-AA secretion from liver. We found that PDGF-AA secretion further stimulates its own expression through protein kinase C activity and contributes to insulin resistance through decreased expression of both insulin receptor substrate 1 and of insulin receptor. Importantly, hepatocyte insulin sensitivity can be restored by PDGF-AA blocking antibodies, PDGF receptor inhibitors and by metformin opening therapeutic avenues. Conclusion: Therefore, in the liver of obese patients with T2D, the increased PDGF-AA signaling contributes to insulin resistance, opening new therapeutic avenues against T2D and NAFLD., Comment: 29 pages 7 figures 1 tables

Published
2017

31. ERRγ Preserves Brown Fat Innate Thermogenic Activity

Author

Ahmadian, Maryam, Liu, Sihao, Reilly, Shannon M, Hah, Nasun, Fan, Weiwei, Yoshihara, Eiji, Jha, Pooja, De Magalhaes Filho, C Daniel, Jacinto, Sandra, Gomez, Andrew V, Dai, Yang, Yu, Ruth T, Liddle, Christopher, Atkins, Annette R, Auwerx, Johan, Saltiel, Alan R, Downes, Michael, and Evans, Ronald M

Subjects
Biochemistry and Cell Biology, Biological Sciences, Nutrition, Genetics, Obesity, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Metabolic and endocrine, Adipose Tissue, Brown, Animals, Energy Metabolism, Mice, Receptors, Estrogen, Thermogenesis, BAT, brown adipocyte, brown fat, estrogen related receptor gamma, thermogenesis, thermoneutrality, Medical Physiology, Biological sciences
Abstract

Brown adipose tissue (BAT) adaptively transfers energy from glucose and fat into heat by inducing a gene network that uncouples mitochondrial electron transport. However, the innate transcription factors that enable the rapid adaptive response of BAT are unclear. Here, we identify estrogen-related receptor gamma (ERRγ) as a critical factor for maintaining BAT identity. ERRγ is selectively expressed in BAT versus WAT, in which, in the absence of PGC1α, it drives a signature transcriptional network of thermogenic and oxidative genes in the basal (i.e., thermoneutral) state. Mice lacking ERRγ in adipose tissue (ERRγKO mice) display marked downregulation of BAT-selective genes that leads to a pronounced whitening of BAT. Consistent with the transcriptional changes, the thermogenic capacity of ERRγKO mice is severely blunted, such that they fail to survive an acute cold challenge. These findings reveal a role for ERRγ as a critical thermoneutral maintenance factor required to prime BAT for thermogenesis.

Published
2018

32. GRAM domain proteins specialize functionally distinct ER-PM contact sites in human cells.

Author

Besprozvannaya, Marina, Dickson, Eamonn, Li, Hao, Ginburg, Kenneth S, Bers, Donald M, Auwerx, Johan, and Nunnari, Jodi

Subjects
Cell Line, Cell Membrane, Endoplasmic Reticulum, Animals, Humans, Calcium, Phosphatidylinositol Phosphates, Membrane Proteins, Neoplasm Proteins, Homeostasis, Synaptotagmins, Stromal Interaction Molecule 1, ER-PM contact sites, GRAMD proteins, PIP lipids, cell biology, cortical ER, human, membrane contact site, store operated calcium entry, 1.1 Normal biological development and functioning, Generic Health Relevance, Biochemistry and Cell Biology
Abstract

Endoplasmic reticulum (ER) membrane contact sites (MCSs) are crucial regulatory hubs in cells, playing roles in signaling, organelle dynamics, and ion and lipid homeostasis. Previous work demonstrated that the highly conserved yeast Ltc/Lam sterol transporters localize and function at ER MCSs. Our analysis of the human family members, GRAMD1a and GRAMD2a, demonstrates that they are ER-PM MCS proteins, which mark separate regions of the plasma membrane (PM) and perform distinct functions in vivo. GRAMD2a, but not GRAMD1a, co-localizes with the E-Syt2/3 tethers at ER-PM contacts in a PIP lipid-dependent manner and pre-marks the subset of PI(4,5)P2-enriched ER-PM MCSs utilized for STIM1 recruitment. Data from an analysis of cells lacking GRAMD2a suggest that it is an organizer of ER-PM MCSs with pleiotropic functions including calcium homeostasis. Thus, our data demonstrate the existence of multiple ER-PM domains in human cells that are functionally specialized by GRAM-domain containing proteins.

Published
2018

37. Metabolic Rewiring by Loss of Sirt5 Promotes Kras-Induced Pancreatic Cancer Progression

Author

Hu, Tuo, Shukla, Surendra K., Vernucci, Enza, He, Chunbo, Wang, Dezhen, King, Ryan J., Jha, Kanupriya, Siddhanta, Kasturi, Mullen, Nicholas J., Attri, Kuldeep S., Murthy, Divya, Chaika, Nina V., Thakur, Ravi, Mulder, Scott E., Pacheco, Camila G., Fu, Xiao, High, Robin R., Yu, Fang, Lazenby, Audrey, Steegborn, Clemens, Lan, Ping, Mehla, Kamiya, Rotili, Dante, Chaudhary, Sarika, Valente, Sergio, Tafani, Marco, Mai, Antonello, Auwerx, Johan, Verdin, Eric, Tuveson, David, and Singh, Pankaj K.

Published
2021
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39. Intestinal NCoR1, a regulator of epithelial cell maturation, controls neonatal hyperbilirubinemia

Author

Chen, Shujuan, Lu, Wenqi, Yueh, Mei-Fei, Rettenmeier, Eva, Liu, Miao, Paszek, Miles, Auwerx, Johan, Yu, Ruth T, Evans, Ronald M, Wang, Kepeng, Karin, Michael, and Tukey, Robert H

Subjects
Paediatrics, Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Liver Disease, Genetics, Pediatric, Digestive Diseases, Perinatal Period - Conditions Originating in Perinatal Period, 2.1 Biological and endogenous factors, Reproductive health and childbirth, Animals, Animals, Newborn, Bilirubin, Epithelial Cells, Glucuronosyltransferase, Humans, Hyperbilirubinemia, Neonatal, I-kappa B Kinase, Intestinal Mucosa, Liver, Mice, Nuclear Receptor Co-Repressor 1, humanized UGT1 mice, UDP-glucuronosyltransferase 1A1, IKK beta, kernicterus, encephalopathy, IKKβ
Abstract

Severe neonatal hyperbilirubinemia (SNH) and the onset of bilirubin encephalopathy and kernicterus result in part from delayed expression of UDP-glucuronosyltransferase 1A1 (UGT1A1) and the inability to metabolize bilirubin. Although there is a good understanding of the early events after birth that lead to the rapid increase in serum bilirubin, the events that control delayed expression of UGT1A1 during development remain a mystery. Humanized UGT1 (hUGT1) mice develop SNH spontaneously, which is linked to repression of both liver and intestinal UGT1A1. In this study, we report that deletion of intestinal nuclear receptor corepressor 1 (NCoR1) completely diminishes hyperbilirubinemia in hUGT1 neonates because of intestinal UGT1A1 gene derepression. Transcriptomic studies and immunohistochemistry analysis demonstrate that NCoR1 plays a major role in repressing developmental maturation of the intestines. Derepression is marked by accelerated metabolic and oxidative phosphorylation, drug metabolism, fatty acid metabolism, and intestinal maturation, events that are controlled predominantly by H3K27 acetylation. The control of NCoR1 function and derepression is linked to IKKβ function, as validated in hUGT1 mice with targeted deletion of intestinal IKKβ. Physiological events during neonatal development that target activation of an IKKβ/NCoR1 loop in intestinal epithelial cells lead to derepression of genes involved in intestinal maturation and bilirubin detoxification. These findings provide a mechanism of NCoR1 in intestinal homeostasis during development and provide a key link to those events that control developmental repression of UGT1A1 and hyperbilirubinemia.

Published
2017

40. Gene-by-environment modulation of lifespan and weight gain in the murine BXD family

Author

Roy, Suheeta, Sleiman, Maroun Bou, Jha, Pooja, Ingels, Jesse F., Chapman, Casey J., McCarty, Melinda S., Ziebarth, Jesse D., Hook, Michael, Sun, Anna, Zhao, Wenyuan, Huang, Jinsong, Neuner, Sarah M., Wilmott, Lynda A., Shapaker, Thomas M., Centeno, Arthur G., Ashbrook, David G., Mulligan, Megan K., Kaczorowski, Catherine C., Makowski, Liza, Cui, Yan, Read, Robert W., Miller, Richard A., Mozhui, Khyobeni, Williams, Evan G., Sen, Saunak, Lu, Lu, Auwerx, Johan, and Williams, Robert W.

Published
2021
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49. Nicotinamide riboside supplementation alters body composition and skeletal muscle acetylcarnitine concentrations in healthy obese humans

Author

Remie, Carlijn ME, Roumans, Kay HM, Moonen, Michiel PB, Connell, Niels J, Havekes, Bas, Mevenkamp, Julian, Lindeboom, Lucas, de Wit, Vera HW, van de Weijer, Tineke, Aarts, Suzanne ABM, Lutgens, Esther, Schomakers, Bauke V, Elfrink, Hyung L, Zapata-Pérez, Rubén, Houtkooper, Riekelt H, Auwerx, Johan, Hoeks, Joris, Schrauwen-Hinderling, Vera B, Phielix, Esther, and Schrauwen, Patrick

Published
2020
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