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Qinglei Yin Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Liyun Shen Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Yicheng Qi Division of Endocrinology and Metabolism, Department of Internal Medicine, RenJi Hospital, Shanghai Jiao-Tong University School of Medicine, Pudong, Shanghai, China

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Dalong Song Reproductive Medicine Center, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Science, Guangzhou, China

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Lei Ye Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Ying Peng Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Yanqiu Wang Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Zhou Jin Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Guang Ning Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Weiqing Wang Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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Dongping Lin Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital, Affiliated Shanghai Jiao-Tong University School of Medicine, Shanghai, China

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Shu Wang Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Institute of EndocrineRuijin Hospital, Shanghai Jiao-Tong University School of Medicine, China

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. 2009 , Gao et al. 2012 , Kong et al. 2011 ). Moreover, SIRT1 is a critical suppressor of T-cell immunity that acts by suppressing the activity of transcription factors, such as nuclear factor kappa light chain enhancer of activated B cells (NF

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Karen Piper Hanley
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Tom Hearn Endocrinology and Diabetes Group, Human Genetics Division, Beta-Cell Development and Function Group, Peninsula Medical School, Manchester Academic Health Science Centre, University of Manchester, A V Hill Building, Oxford Road, Manchester M13 9PT, UK

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Andrew Berry
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Melanie J Carvell Endocrinology and Diabetes Group, Human Genetics Division, Beta-Cell Development and Function Group, Peninsula Medical School, Manchester Academic Health Science Centre, University of Manchester, A V Hill Building, Oxford Road, Manchester M13 9PT, UK

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Ann-Marie Patch Endocrinology and Diabetes Group, Human Genetics Division, Beta-Cell Development and Function Group, Peninsula Medical School, Manchester Academic Health Science Centre, University of Manchester, A V Hill Building, Oxford Road, Manchester M13 9PT, UK

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Louise J Williams Endocrinology and Diabetes Group, Human Genetics Division, Beta-Cell Development and Function Group, Peninsula Medical School, Manchester Academic Health Science Centre, University of Manchester, A V Hill Building, Oxford Road, Manchester M13 9PT, UK

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Sarah A Sugden
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David I Wilson Endocrinology and Diabetes Group, Human Genetics Division, Beta-Cell Development and Function Group, Peninsula Medical School, Manchester Academic Health Science Centre, University of Manchester, A V Hill Building, Oxford Road, Manchester M13 9PT, UK

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Sian Ellard Endocrinology and Diabetes Group, Human Genetics Division, Beta-Cell Development and Function Group, Peninsula Medical School, Manchester Academic Health Science Centre, University of Manchester, A V Hill Building, Oxford Road, Manchester M13 9PT, UK

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Neil A Hanley
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give rise to the adult cell lineages, including β-cells ( Murtaugh 2007 ). Experiments manipulating genes in mice have discovered a multitude of transcription factors that regulate this transition ( Wilson et al . 2003 ). Within a subset of progenitors

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Nan Yang Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Giorgio Caratti Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Louise M Ince Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Toryn M Poolman Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Peter J Trebble Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Cathy M Holt Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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David W Ray Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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Laura C Matthews Manchester Centre for Nuclear Hormone Research in Disease and Institute of Human Development, Institute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK

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synthetic Gc molecules modulate the activity of the near ubiquitously expressed glucocorticoid receptor (GR). The GR is a member of the nuclear hormone receptor superfamily and acts as a ligand-inducible transcription factor by interacting with chromatin to

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Young Hoon Son Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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Seok-Jin Lee Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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Ki-Baek Lee Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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Jin-Haeng Lee Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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Eui Man Jeong Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea
Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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Sun Gun Chung Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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Sang-Chul Park Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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In-Gyu Kim Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea
Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea

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al . 2011 ). In contrast, MAFbx/Atrogin1 suppresses protein synthesis through the ubiquitination and degradation of eIF3f and MyoD, key factors regulating translation and transcription in muscle respectively ( Attaix & Baracos 2010 ). Results

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Yanli Miao Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Haojie Qin Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Yi Zhong Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Kai Huang Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Caijun Rao Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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asprosin mediated inhibition of adipose browning To uncover the underlying mechanism of the aforementioned observations, we explored whether Nrf2, a crucial antioxidant transcription factor, was involved in the process. Nrf2 is a transcription factor

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Joachim M Weitzel Institute of Reproductive Biology, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Torsten Viergutz Institute of Reproductive Biology, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Dirk Albrecht Institute of Microbiology, Ernst-Moritz-Arndt-University, Greifswald, Germany

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Rupert Bruckmaier Veterinary Physiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland

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Marion Schmicke Clinic for Cattle, Endocrinology Laboratory, University of Veterinary Medicine Hannover, Hannover, Germany

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Armin Tuchscherer Institute of Genetics and Biometry, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Franziska Koch Institute of Nutritional Physiology ‘Oskar Kellner’, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Björn Kuhla Institute of Nutritional Physiology ‘Oskar Kellner’, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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, Weitzel & Iwen 2011 ). The THRs belong to a group of transcription factors whose gene regulation function is depending on the presence or absence of their particular ligand (i.e. TH). Liganded and un-liganded THRs recruit cofactors which convert chromatin

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Tina Seidu Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Patrick McWhorter Department of Chemistry, Youngstown State University, Youngstown, Ohio, USA

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Jessie Myer Department of Biology, University of Missouri, Columbia, Missouri, USA

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Rabita Alamgir Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Nicole Eregha Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Dilip Bogle Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Taylor Lofton Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Carolyn Ecelbarger Department of Medicine, Georgetown University Medical Center, Washington, DC, USA

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Stanley Andrisse Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA
Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA

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level ( Berlanga et al. 2014 ). Nuclear transcription factors (Liver X receptor (LxRα), sterol regulatory element-binding protein 1c (SREBP1c), carbohydrate-responsive element-binding protein (ChREBP), and farnesoid X receptor (FxR) and enzymes ACC1

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M A Hyatt Early Life Nutrition Research Unit, Respiratory Biomedical Research Unit, Department of Animal Sciences, Division of Human Development, Academic Child Health

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D H Keisler Early Life Nutrition Research Unit, Respiratory Biomedical Research Unit, Department of Animal Sciences, Division of Human Development, Academic Child Health

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H Budge Early Life Nutrition Research Unit, Respiratory Biomedical Research Unit, Department of Animal Sciences, Division of Human Development, Academic Child Health
Early Life Nutrition Research Unit, Respiratory Biomedical Research Unit, Department of Animal Sciences, Division of Human Development, Academic Child Health

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M E Symonds Early Life Nutrition Research Unit, Respiratory Biomedical Research Unit, Department of Animal Sciences, Division of Human Development, Academic Child Health
Early Life Nutrition Research Unit, Respiratory Biomedical Research Unit, Department of Animal Sciences, Division of Human Development, Academic Child Health

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process that requires coordinated communication between hormones, growth factors and transcription factors. Glucocorticoids, for example, are major stimulators of adipose tissue development and fat accumulation especially in combination with insulin

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Bettina Geidl-Flueck Department of Endocrinology, Diabetology and Clinical Nutrition, University Hospital Zurich (USZ) and University of Zurich (UZH), Switzerland

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Philipp A Gerber Department of Endocrinology, Diabetology and Clinical Nutrition, University Hospital Zurich (USZ) and University of Zurich (UZH), Switzerland

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hepatocytes. DNL contributes to the maintenance of glucose homeostasis. A healthy balance of hepatocyte and adipocyte DNL is essential for maintaining systemic insulin sensitivity ( Song et al. 2018 ). The master transcription factors sterol

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Ryoko Yamamoto Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Tomoko Minamizaki Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Yuji Yoshiko Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Hirotaka Yoshioka Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Kazuo Tanne Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Jane E Aubin Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Norihiko Maeda Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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-resistant rickets suggest the existence of additional phosphaturic factor(s). Recently, intensive studies of several such putative factors (e.g. matrix extracellular phosphoglycoprotein, dentin matrix protein 1 (DMP1), and fibroblast growth factor 23 (FGF23) have

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