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Eric N. Olson

Kelly M Anderson, Douglas M Anderson, John R McAnally, John M Shelton, Rhonda Bassel-Duby, Eric N Olson
HAND2 is an ancestral regulator of heart development and one of four transcription factors that control the reprogramming of fibroblasts into cardiomyocytes. Deletion of Hand2 in mice results in right ventricle hypoplasia and embryonic lethality. Hand2 expression is tightly regulated by upstream enhancers that reside within a super-enhancer delineated by histone H3 acetyl Lys27 (H3K27ac) modifications. Here we show that transcription of a Hand2-associated long non-coding RNA, which we named upperhand (Uph), is required to maintain the super-enhancer signature and elongation of RNA polymerase II through the Hand2 enhancer locus...
October 26, 2016: Nature
Na Li, Lakshman Subrahmanyan, Emily Smith, Xiaoqing Yu, Samir Zaidi, Murim Choi, Shrikant Mane, Carol Nelson-Williams, Mohaddeseh Behjati, Mohammad Kazemi, Mohammad Hashemi, Mohsen Fathzadeh, Anand Narayanan, Likun Tian, Farhad Montazeri, Mitra Mani, Michael L Begleiter, Brian G Coon, Henry T Lynch, Eric N Olson, Hongyu Zhao, Jürgen Ruland, Richard P Lifton, Arya Mani
No abstract text is available yet for this article.
October 6, 2016: American Journal of Human Genetics
Chengzu Long, Leonela Amoasii, Rhonda Bassel-Duby, Eric N Olson
Importance: Muscle weakness, the most common symptom of neuromuscular disease, may result from muscle dysfunction or may be caused indirectly by neuronal and neuromuscular junction abnormalities. To date, more than 780 monogenic neuromuscular diseases, linked to 417 different genes, have been identified in humans. Genome-editing methods, especially the CRISPR (clustered regularly interspaced short palindromic repeats)-Cas9 (CRISPR-associated protein 9) system, hold clinical potential for curing many monogenic disorders, including neuromuscular diseases such as Duchenne muscular dystrophy, spinal muscular atrophy, amyotrophic lateral sclerosis, and myotonic dystrophy type 1...
September 26, 2016: JAMA Neurology
Jijing Tian, Guoxiang Yang, Huan-Yuan Chen, Daniel K Hsu, Alexey Tomilov, Kristin A Olson, Ali Dehnad, Sarah R Fish, Gino Cortopassi, Bin Zhao, Fu-Tong Liu, M Eric Gershwin, Natalie J Török, Joy X Jiang
Macrophage activation is an important feature of primary biliary cholangitis (PBC) pathogenesis and other cholestatic liver diseases. Galectin-3 (Gal3), a pleiotropic lectin, is produced by monocytic cells and macrophages. However, its role in PBC has not been addressed. We hypothesized that Gal3 is a key to induce NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome in macrophages and in turn to propagate proinflammatory IL-17 signaling. In liver tissues from patients with PBC and dnTGF-βRII mice, a model of autoimmune cholangitis, the expression of Gal3, NLRP3, and the adaptor protein adaptor apoptosis-associated speck-like protein was induced, with the downstream activation of caspase-1 and IL-1β...
September 14, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Alexander Polster, Benjamin R Nelson, Eric N Olson, Kurt G Beam
In skeletal muscle, conformational coupling between CaV1.1 in the plasma membrane and type 1 ryanodine receptor (RyR1) in the sarcoplasmic reticulum (SR) is thought to underlie both excitation-contraction (EC) coupling Ca(2+) release from the SR and retrograde coupling by which RyR1 increases the magnitude of the Ca(2+) current via CaV1.1. Recent work has shown that EC coupling fails in muscle from mice and fish null for the protein Stac3 (SH3 and cysteine-rich domain 3) but did not establish the functional role of Stac3 in the CaV1...
September 27, 2016: Proceedings of the National Academy of Sciences of the United States of America
Mingfeng Zhang, Zhaoming Wang, Ofure Obazee, Jinping Jia, Erica J Childs, Jason Hoskins, Gisella Figlioli, Evelina Mocci, Irene Collins, Charles C Chung, Christopher Hautman, Alan A Arslan, Laura Beane-Freeman, Paige M Bracci, Julie Buring, Eric J Duell, Steven Gallinger, Graham G Giles, Gary E Goodman, Phyllis J Goodman, Aruna Kamineni, Laurence N Kolonel, Matthew H Kulke, Núria Malats, Sara H Olson, Howard D Sesso, Kala Visvanathan, Emily White, Wei Zheng, Christian C Abnet, Demetrius Albanes, Gabriella Andreotti, Lauren Brais, H Bas Bueno-de-Mesquita, Daniela Basso, Sonja I Berndt, Marie-Christine Boutron-Ruault, Maarten F Bijlsma, Hermann Brenner, Laurie Burdette, Daniele Campa, Neil E Caporaso, Gabriele Capurso, Giulia Martina Cavestro, Michelle Cotterchio, Eithne Costello, Joanne Elena, Ugo Boggi, J Michael Gaziano, Maria Gazouli, Edward L Giovannucci, Michael Goggins, Myron Gross, Christopher A Haiman, Manal Hassan, Kathy J Helzlsouer, Nan Hu, David J Hunter, Elzbieta Iskierka-Jazdzewska, Mazda Jenab, Rudolf Kaaks, Timothy J Key, Kay-Tee Khaw, Eric A Klein, Manolis Kogevinas, Vittorio Krogh, Juozas Kupcinskas, Robert C Kurtz, Maria T Landi, Stefano Landi, Loic Le Marchand, Andrea Mambrini, Satu Mannisto, Roger L Milne, Rachel E Neale, Ann L Oberg, Salvatore Panico, Alpa V Patel, Petra H M Peeters, Ulrike Peters, Raffaele Pezzilli, Miquel Porta, Mark Purdue, J Ramón Quiros, Elio Riboli, Nathaniel Rothman, Aldo Scarpa, Ghislaine Scelo, Xiao-Ou Shu, Debra T Silverman, Pavel Soucek, Oliver Strobel, Malin Sund, Ewa Małecka-Panas, Philip R Taylor, Francesca Tavano, Ruth C Travis, Mark Thornquist, Anne Tjønneland, Geoffrey S Tobias, Dimitrios Trichopoulos, Yogesh Vashist, Pavel Vodicka, Jean Wactawski-Wende, Nicolas Wentzensen, Herbert Yu, Kai Yu, Anne Zeleniuch-Jacquotte, Charles Kooperberg, Harvey A Risch, Eric J Jacobs, Donghui Li, Charles Fuchs, Robert Hoover, Patricia Hartge, Stephen J Chanock, Gloria M Petersen, Rachael S Stolzenberg-Solomon, Brian M Wolpin, Peter Kraft, Alison P Klein, Federico Canzian, Laufey T Amundadottir
Genome-wide association studies (GWAS) have identified common pancreatic cancer susceptibility variants at 13 chromosomal loci in individuals of European descent. To identify new susceptibility variants, we performed imputation based on 1000 Genomes (1000G) Project data and association analysis using 5,107 case and 8,845 control subjects from 27 cohort and case-control studies that participated in the PanScan I-III GWAS. This analysis, in combination with a two-staged replication in an additional 6,076 case and 7,555 control subjects from the PANcreatic Disease ReseArch (PANDoRA) and Pancreatic Cancer Case-Control (PanC4) Consortia uncovered 3 new pancreatic cancer risk signals marked by single nucleotide polymorphisms (SNPs) rs2816938 at chromosome 1q32...
August 1, 2016: Oncotarget
Dörte Lodka, Aanchal Pahuja, Cornelia Geers-Knörr, Renate J Scheibe, Marcel Nowak, Jida Hamati, Clemens Köhncke, Bettina Purfürst, Tamara Kanashova, Sibylle Schmidt, David J Glass, Ingo Morano, Arnd Heuser, Theresia Kraft, Rhonda Bassel-Duby, Eric N Olson, Gunnar Dittmar, Thomas Sommer, Jens Fielitz
BACKGROUND: The Muscle-specific RING-finger (MuRF) protein family of E3 ubiquitin ligases is important for maintenance of muscular structure and function. MuRF proteins mediate adaptation of striated muscles to stress. MuRF2 and MuRF3 bind to microtubules and are implicated in sarcomere formation with noticeable functional redundancy. However, if this redundancy is important for muscle function in vivo is unknown. Our objective was to investigate cooperative function of MuRF2 and MuRF3 in the skeletal muscle and the heart in vivo...
May 2016: Journal of Cachexia, Sarcopenia and Muscle
Douglas M Anderson, Jessica Cannavino, Hui Li, Kelly M Anderson, Benjamin R Nelson, John McAnally, Svetlana Bezprozvannaya, Yun Liu, Weichun Lin, Ning Liu, Rhonda Bassel-Duby, Eric N Olson
Innervation of skeletal muscle by motor neurons occurs through the neuromuscular junction, a cholinergic synapse essential for normal muscle growth and function. Defects in nerve-muscle signaling cause a variety of neuromuscular disorders with features of ataxia, paralysis, skeletal muscle wasting, and degeneration. Here we show that the nuclear zinc finger protein ZFP106 is highly enriched in skeletal muscle and is required for postnatal maintenance of myofiber innervation by motor neurons. Genetic disruption of Zfp106 in mice results in progressive ataxia and hindlimb paralysis associated with motor neuron degeneration, severe muscle wasting, and premature death by 6 mo of age...
August 2, 2016: Proceedings of the National Academy of Sciences of the United States of America
Bercin K Cenik, Ning Liu, Beibei Chen, Svetlana Bezprozvannaya, Eric N Olson, Rhonda Bassel-Duby
Myocardin-related transcription factors (MRTFs) play a central role in the regulation of actin expression and cytoskeletal dynamics. Stimuli that promote actin polymerization allow for shuttling of MRTFs to the nucleus where they activate serum response factor (SRF), a regulator of actin and other cytoskeletal protein genes. SRF is an essential regulator of skeletal muscle differentiation and numerous components of the muscle sarcomere, but the potential involvement of MRTFs in skeletal muscle development has not been examined...
August 1, 2016: Development
Da-Hye Lee, Jae Oh Park, Tae-Shin Kim, Sang-Kyum Kim, Tack-Hoon Kim, Min-Chul Kim, Gun Soo Park, Jeong-Hwan Kim, Shinji Kuninaka, Eric N Olson, Hideyuki Saya, Seon-Young Kim, Ho Lee, Dae-Sik Lim
The Hippo pathway regulates the self-renewal and differentiation of various adult stem cells, but its role in cell fate determination and differentiation during liver development remains unclear. Here we report that the Hippo pathway controls liver cell lineage specification and proliferation separately from Notch signalling, using mice and primary hepatoblasts with liver-specific knockout of Lats1 and Lats2 kinase, the direct upstream regulators of YAP and TAZ. During and after liver development, the activation of YAP/TAZ induced by loss of Lats1/2 forces hepatoblasts or hepatocytes to commit to the biliary epithelial cell (BEC) lineage...
2016: Nature Communications
Liguo Zhang, Xuelian He, Lei Liu, Minqing Jiang, Chuntao Zhao, Haibo Wang, Danyang He, Tao Zheng, Xianyao Zhou, Aishlin Hassan, Zhixing Ma, Mei Xin, Zheng Sun, Mitchell A Lazar, Steven A Goldman, Eric N Olson, Q Richard Lu
No abstract text is available yet for this article.
June 20, 2016: Developmental Cell
Mitchell J Machiela, Weiyin Zhou, Eric Karlins, Joshua N Sampson, Neal D Freedman, Qi Yang, Belynda Hicks, Casey Dagnall, Christopher Hautman, Kevin B Jacobs, Christian C Abnet, Melinda C Aldrich, Christopher Amos, Laufey T Amundadottir, Alan A Arslan, Laura E Beane-Freeman, Sonja I Berndt, Amanda Black, William J Blot, Cathryn H Bock, Paige M Bracci, Louise A Brinton, H Bas Bueno-de-Mesquita, Laurie Burdett, Julie E Buring, Mary A Butler, Federico Canzian, Tania Carreón, Kari G Chaffee, I-Shou Chang, Nilanjan Chatterjee, Chu Chen, Constance Chen, Kexin Chen, Charles C Chung, Linda S Cook, Marta Crous Bou, Michael Cullen, Faith G Davis, Immaculata De Vivo, Ti Ding, Jennifer Doherty, Eric J Duell, Caroline G Epstein, Jin-Hu Fan, Jonine D Figueroa, Joseph F Fraumeni, Christine M Friedenreich, Charles S Fuchs, Steven Gallinger, Yu-Tang Gao, Susan M Gapstur, Montserrat Garcia-Closas, Mia M Gaudet, J Michael Gaziano, Graham G Giles, Elizabeth M Gillanders, Edward L Giovannucci, Lynn Goldin, Alisa M Goldstein, Christopher A Haiman, Goran Hallmans, Susan E Hankinson, Curtis C Harris, Roger Henriksson, Elizabeth A Holly, Yun-Chul Hong, Robert N Hoover, Chao A Hsiung, Nan Hu, Wei Hu, David J Hunter, Amy Hutchinson, Mazda Jenab, Christoffer Johansen, Kay-Tee Khaw, Hee Nam Kim, Yeul Hong Kim, Young Tae Kim, Alison P Klein, Robert Klein, Woon-Puay Koh, Laurence N Kolonel, Charles Kooperberg, Peter Kraft, Vittorio Krogh, Robert C Kurtz, Andrea LaCroix, Qing Lan, Maria Teresa Landi, Loic Le Marchand, Donghui Li, Xiaolin Liang, Linda M Liao, Dongxin Lin, Jianjun Liu, Jolanta Lissowska, Lingeng Lu, Anthony M Magliocco, Nuria Malats, Keitaro Matsuo, Lorna H McNeill, Robert R McWilliams, Beatrice S Melin, Lisa Mirabello, Lee Moore, Sara H Olson, Irene Orlow, Jae Yong Park, Ana Patiño-Garcia, Beata Peplonska, Ulrike Peters, Gloria M Petersen, Loreall Pooler, Jennifer Prescott, Ludmila Prokunina-Olsson, Mark P Purdue, You-Lin Qiao, Preetha Rajaraman, Francisco X Real, Elio Riboli, Harvey A Risch, Benjamin Rodriguez-Santiago, Avima M Ruder, Sharon A Savage, Fredrick Schumacher, Ann G Schwartz, Kendra L Schwartz, Adeline Seow, Veronica Wendy Setiawan, Gianluca Severi, Hongbing Shen, Xin Sheng, Min-Ho Shin, Xiao-Ou Shu, Debra T Silverman, Margaret R Spitz, Victoria L Stevens, Rachael Stolzenberg-Solomon, Daniel Stram, Ze-Zhong Tang, Philip R Taylor, Lauren R Teras, Geoffrey S Tobias, David Van Den Berg, Kala Visvanathan, Sholom Wacholder, Jiu-Cun Wang, Zhaoming Wang, Nicolas Wentzensen, William Wheeler, Emily White, John K Wiencke, Brian M Wolpin, Maria Pik Wong, Chen Wu, Tangchun Wu, Xifeng Wu, Yi-Long Wu, Jay S Wunder, Lucy Xia, Hannah P Yang, Pan-Chyr Yang, Kai Yu, Krista A Zanetti, Anne Zeleniuch-Jacquotte, Wei Zheng, Baosen Zhou, Regina G Ziegler, Luis A Perez-Jurado, Neil E Caporaso, Nathaniel Rothman, Margaret Tucker, Michael C Dean, Meredith Yeager, Stephen J Chanock
To investigate large structural clonal mosaicism of chromosome X, we analysed the SNP microarray intensity data of 38,303 women from cancer genome-wide association studies (20,878 cases and 17,425 controls) and detected 124 mosaic X events >2 Mb in 97 (0.25%) women. Here we show rates for X-chromosome mosaicism are four times higher than mean autosomal rates; X mosaic events more often include the entire chromosome and participants with X events more likely harbour autosomal mosaic events. X mosaicism frequency increases with age (0...
2016: Nature Communications
Vijay Ramaswamy, Thomas Hielscher, Stephen C Mack, Alvaro Lassaletta, Tong Lin, Kristian W Pajtler, David T W Jones, Betty Luu, Florence M G Cavalli, Kenneth Aldape, Marc Remke, Martin Mynarek, Stefan Rutkowski, Sridharan Gururangan, Roger E McLendon, Eric S Lipp, Christopher Dunham, Juliette Hukin, David D Eisenstat, Dorcas Fulton, Frank K H van Landeghem, Mariarita Santi, Marie-Lise C van Veelen, Erwin G Van Meir, Satoru Osuka, Xing Fan, Karin M Muraszko, Daniela P C Tirapelli, Sueli M Oba-Shinjo, Suely K N Marie, Carlos G Carlotti, Ji Yeoun Lee, Amulya A Nageswara Rao, Caterina Giannini, Claudia C Faria, Sofia Nunes, Jaume Mora, Ronald L Hamilton, Peter Hauser, Nada Jabado, Kevin Petrecca, Shin Jung, Luca Massimi, Massimo Zollo, Giuseppe Cinalli, László Bognár, Almos Klekner, Tibor Hortobágyi, Sarah Leary, Ralph P Ermoian, James M Olson, Jeffrey R Leonard, Corrine Gardner, Wieslawa A Grajkowska, Lola B Chambless, Jason Cain, Charles G Eberhart, Sama Ahsan, Maura Massimino, Felice Giangaspero, Francesca R Buttarelli, Roger J Packer, Lyndsey Emery, William H Yong, Horacio Soto, Linda M Liau, Richard Everson, Andrew Grossbach, Tarek Shalaby, Michael Grotzer, Matthias A Karajannis, David Zagzag, Helen Wheeler, Katja von Hoff, Marta M Alonso, Teresa Tuñon, Ulrich Schüller, Karel Zitterbart, Jaroslav Sterba, Jennifer A Chan, Miguel Guzman, Samer K Elbabaa, Howard Colman, Girish Dhall, Paul G Fisher, Maryam Fouladi, Amar Gajjar, Stewart Goldman, Eugene Hwang, Marcel Kool, Harshad Ladha, Elizabeth Vera-Bolanos, Khalida Wani, Frank Lieberman, Tom Mikkelsen, Antonio M Omuro, Ian F Pollack, Michael Prados, H Ian Robins, Riccardo Soffietti, Jing Wu, Phillipe Metellus, Uri Tabori, Ute Bartels, Eric Bouffet, Cynthia E Hawkins, James T Rutka, Peter Dirks, Stefan M Pfister, Thomas E Merchant, Mark R Gilbert, Terri S Armstrong, Andrey Korshunov, David W Ellison, Michael D Taylor
PURPOSE: Posterior fossa ependymoma comprises two distinct molecular variants termed EPN_PFA and EPN_PFB that have a distinct biology and natural history. The therapeutic value of cytoreductive surgery and radiation therapy for posterior fossa ependymoma after accounting for molecular subgroup is not known. METHODS: Four independent nonoverlapping retrospective cohorts of posterior fossa ependymomas (n = 820) were profiled using genome-wide methylation arrays. Risk stratification models were designed based on known clinical and newly described molecular biomarkers identified by multivariable Cox proportional hazards analyses...
July 20, 2016: Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology
Ge Tao, Peter C Kahr, Yuka Morikawa, Min Zhang, Mahdis Rahmani, Todd R Heallen, Lele Li, Zhao Sun, Eric N Olson, Brad A Amendt, James F Martin
Myocardial infarction results in compromised myocardial function and heart failure owing to insufficient cardiomyocyte self-renewal. Unlike many vertebrates, mammalian hearts have only a transient neonatal renewal capacity. Reactivating primitive reparative ability in the mature mammalian heart requires knowledge of the mechanisms that promote early heart repair. By testing an established Hippo-deficient heart regeneration mouse model for factors that promote renewal, here we show that the expression of Pitx2 is induced in injured, Hippo-deficient ventricles...
May 25, 2016: Nature
Kenneth N Cameron, Patricia Reed, David B Morgan, Alain I Ondzié, Crickette M Sanz, Hjalmar S Kühl, Sarah H Olson, Eric Leroy, William B Karesh, Roger Mundry
In 2006-2007 we observed an unusual mortality event among apes in northern Republic of Congo that, although not diagnostically confirmed, we believe to have been a disease outbreak. In 2007-2011 we conducted ape nest surveys in the region, recording 11,835 G. g. gorilla nests (2,262 groups) and 5,548 P. t. troglodytes nests (2,139 groups). We developed a statistical model to determine likely points of origin of the outbreak to help identify variables associated with disease emergence and spread. We modeled disease spread across the study area, using suitable habitat conditions for apes as proxy for local ape densities...
2016: PloS One
Na Li, Lakshman Subrahmanyan, Emily Smith, Xiaoqing Yu, Samir Zaidi, Murim Choi, Shrikant Mane, Carol Nelson-Williams, Mohadesseh Bahjati, Mohammad Kazemi, Mohammad Hashemi, Mohsen Fathzadeh, Anand Narayanan, Likun Tian, Farhad Montazeri, Mitra Mani, Michael L Begleiter, Brian G Coon, Henry T Lynch, Eric N Olson, Hongyu Zhao, Jürgen Ruland, Richard P Lifton, Arya Mani
Nonsyndromic patent ductus arteriosus (PDA) is a common congenital heart defect (CHD) with both inherited and acquired causes, but the disease mechanisms have remained elusive. Using combined genome-wide linkage analysis and whole-exome sequencing (WES), we identified independent mutations in PRDM6, which encodes a nuclear protein that is specific to vascular smooth muscle cells (VSMC), has histone methyl transferase activities, and acts as a transcriptional suppressor of contractile proteins. In vitro assays showed that the mutations cause loss of function either by intracellular redistribution of the protein and/or by alteration of its methyltransferase activities...
June 2, 2016: American Journal of Human Genetics
Anamika Singh, Sindhu Ramesh, Dasan Mary Cibi, Lim Sze Yun, Jun Li, Li Li, Lauren J Manderfield, Eric N Olson, Jonathan A Epstein, Manvendra K Singh
Formation of the coronary vasculature is a complex and precisely coordinated morphogenetic process that begins with the formation of epicardium. The epicardium gives rise to many components of the coronary vasculature, including fibroblasts, smooth muscle cells, and endothelium. Hippo signaling components have been implicated in cardiac development and regeneration. However, a role of Hippo signaling in the epicardium has not been explored. Employing a combination of genetic and pharmacological approaches, we demonstrate that inhibition of Hippo signaling mediators Yap and Taz leads to impaired epicardial epithelial-to-mesenchymal transition (EMT) and a reduction in epicardial cell proliferation and differentiation into coronary endothelial cells...
May 17, 2016: Cell Reports
John J Lepore, Eric Olson, Laura Demopoulos, Thomas Haws, Zixing Fang, April M Barbour, Michael Fossler, Victor G Davila-Roman, Stuart D Russell, Robert J Gropler
OBJECTIVES: This study sought to determine if glucagon-like peptide (GLP)-1 ameliorates myocardial metabolic abnormalities in chronic heart failure. BACKGROUND: Albiglutide (GSK716155) is a GLP-1 agonist indicated for type 2 diabetes. METHODS: We performed a randomized, placebo-controlled study evaluating 12 weeks of albiglutide in New York Heart Association II or III subjects with ejection fraction <40%. Subjects received weekly placebo (n = 30) or albiglutide 3...
July 2016: JACC. Heart Failure
Gerard Karsenty, Eric N Olson
Most physiological functions originate with the communication between organs. Mouse genetics has revived this holistic view of physiology through the identification of inter-organ communications that are unanticipated, functionally important, and would have been difficult to uncover otherwise. This Review highlights this point by showing how two tissues usually not seen as endocrine ones, bone and striated muscles, influence several physiological processes in a significant manner.
March 10, 2016: Cell
Dhiraj G Kabra, Katrin Pfuhlmann, Cristina García-Cáceres, Sonja C Schriever, Veronica Casquero García, Adam Fiseha Kebede, Esther Fuente-Martin, Chitrang Trivedi, Kristy Heppner, N Henriette Uhlenhaut, Beata Legutko, Uma D Kabra, Yuanqing Gao, Chun-Xia Yi, Carmelo Quarta, Christoffer Clemmensen, Brian Finan, Timo D Müller, Carola W Meyer, Marcelo Paez-Pereda, Kerstin Stemmer, Stephen C Woods, Diego Perez-Tilve, Robert Schneider, Eric N Olson, Matthias H Tschöp, Paul T Pfluger
Hypothalamic leptin signalling has a key role in food intake and energy-balance control and is often impaired in obese individuals. Here we identify histone deacetylase 5 (HDAC5) as a regulator of leptin signalling and organismal energy balance. Global HDAC5 KO mice have increased food intake and greater diet-induced obesity when fed high-fat diet. Pharmacological and genetic inhibition of HDAC5 activity in the mediobasal hypothalamus increases food intake and modulates pathways implicated in leptin signalling...
2016: Nature Communications
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