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  • thyroid hormone receptor x
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Alies A. van Mullem Department of Internal Medicine, Erasmus University Medical Centre, Rotterdam, The Netherlands

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Theo J. Visser Department of Internal Medicine, Erasmus University Medical Centre, Rotterdam, The Netherlands

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Robin P. Peeters Department of Internal Medicine, Erasmus University Medical Centre, Rotterdam, The Netherlands

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changes in gene expression can be initiated by cytosolic action of the thyroid hormone receptor beta through the phosphatidylinositol 3-kinase pathway. Nucl Recept Signal 2006;4:e020. 10.1621/nrs.04020 16862226 6 Cheng SY: Thyroid hormone receptor

Article Type:
Review Article
DOI:
https://doi.org/10.1159/000360637
Volume/Issue:
Volume 3: Issue 1
Free access
Joachim M. Weitzel Institute of Reproductive Biology, Leibniz Institute for Farm Animal Biology (FBN), FBN Dummerstorf, Dummerstorf, Germany

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Introduction Thyroid hormone (TH) has a profound influence on normal development, differentiation, and metabolism. Genomic actions of THs are mainly mediated and regulated by thyroid hormone receptors (TRs); however, TH-transmitted effects are

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000447232
Volume/Issue:
Volume 5: Issue 3
Free access
Markus Eszlinger Department of Oncology and Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Heritage Medical Research Building, Calgary, Alberta, Canada, and Institute of Pathology, University Hospital Halle, Halle, Germany

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Alexandra Stephenson Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Heritage Medical Research Building, Calgary, Alberta, Canada

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Shideh Mirhadi Program in Cell Biology, Hospital for Sick Children, and Department of Molecular Genetics, University of Toronto, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada

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Konrad Patyra Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland

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Michael F Moran Program in Cell Biology, Hospital for Sick Children, and Department of Molecular Genetics, University of Toronto, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada

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Moosa Khalil Department of Pathology and Laboratory Medicine, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada

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Jukka Kero Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland
Department of Pediatrics, Turku University Hospital, Turku, Finland

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Ralf Paschke Department of Oncology and Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Heritage Medical Research Building, Calgary, Alberta, Canada, and Institute of Pathology, University Hospital Halle, Halle, Germany
Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Heritage Medical Research Building, Calgary, Alberta, Canada
Department of Pathology and Laboratory Medicine, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada
Department of Medicine, Cumming School of Medicine, University of Calgary, Heritage Medical Research Building, Calgary, Alberta, Canada

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Introduction Nonautoimmune hyperthyroidism (NAH) is caused by a constitutively activating thyroid stimulating hormone receptor (TSHR) germline mutation. Germline mutations in TSHR lead to sporadic and familial NAH (SNAH, FNAH) whereas somatic

Article Type:
Research Article
Collections:
Thyroid cancer - basic and translational
DOI:
https://doi.org/10.1530/ETJ-23-0049
Volume/Issue:
Volume 12: Issue 6
Open access
R. Paschke Department of Endocrinology and Nephrology, Leipzig University, Leipzig, Germany

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M. Niedziela Department of Pediatric Endocrinology and Rheumatology, Poznan University of Medical Sciences, Poznan, Poland

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B. Vaidya Department of Endocrinology, Royal Devon and Exeter Hospital, Peninsula Medical School, Exeter, UK

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L. Persani Department of Clinical Sciences, and Community Health, University of Milan, and Istituto Auxologico Italiano, Milan, Italy

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B. Rapoport Autoimmune Disease Unit, Cedars-Sinai Research Institute and School of Medicine, University of California, Los Angeles, Calif., USA

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J. Leclere Centre Hospitalier Universitaire de Nancy, Nancy, France

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a rare thyroid-stimulating hormone receptor activating mutation: case report and literature review. Endocr Pract 2008;14:479–483. 29 Bertalan R, Sallai A, Solyom J, Lotz G, Szabo I, Kovacs B, et al: Hyperthyroidism caused by a germline

Article Type:
Guideline
DOI:
https://doi.org/10.1159/000342982
Volume/Issue:
Volume 1: Issue 3
Free access
Bengt Hallengren Departments of Endocrinology, Skåne University Hospital, Malmö
Department of Clinical Sciences, Lund University, Lund, Sweden

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Tereza Planck Departments of Endocrinology, Skåne University Hospital, Malmö
Department of Clinical Sciences, Lund University, Lund, Sweden

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Peter Åsman Departments of Ophthalmology, Skåne University Hospital, Malmö
Department of Clinical Sciences, Lund University, Lund, Sweden

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Mikael Lantz Departments of Endocrinology, Skåne University Hospital, Malmö
Department of Clinical Sciences, Lund University, Lund, Sweden

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SAT is very rare, and only a limited number of cases of GD occurring after SAT have been reported [ 2 , 3 , 4 , 5 , 6 ]. Here, we report a case of GD with opthalmopathy occurring 11 years after SAT with thyroid-stimulating hormone (TSH) receptor

Article Type:
Case Report
DOI:
https://doi.org/10.1159/000435915
Volume/Issue:
Volume 4: Issue 3
Free access
Manassawee Korwutthikulrangsri Department of Medicine, University of Chicago, Chicago, Illinois, USA
Department of Pediatrics, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand

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Chrysoula Dosiou Department of Medicine, Stanford University School of Medicine, Stanford, California, USA

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Alexandra M. Dumitrescu Department of Medicine, University of Chicago, Chicago, Illinois, USA
Committee on Molecular Metabolism and Nutrition, University of Chicago, Chicago, Illinois, USA

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Samuel Refetoff Department of Medicine, University of Chicago, Chicago, Illinois, USA
Department of Pediatrics, University of Chicago, Chicago, Illinois, USA
Committee on Genetics, University of Chicago, Chicago, Illinois, USA

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What Is Known about This Topic? Mutations in the thyroid hormone receptor beta gene ( THRB ) in the region encoding the T3-binding and the adjacent hinge domains of the receptor have been reported to cause resistance to thyroid hormone

Article Type:
Case Report
DOI:
https://doi.org/10.1159/000503860
Volume/Issue:
Volume 8: Issue 6
Free access
Yalan Hu Department of Laboratory Medicine, Endocrine Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands
Amsterdam Gastroenterology, Endocrinology & Metabolism (AGEM) Research Institute, Amsterdam UMC, Amsterdam, the Netherlands

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Kim Falize Department of Laboratory Medicine, Endocrine Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands

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A S Paul van Trotsenburg Amsterdam Gastroenterology, Endocrinology & Metabolism (AGEM) Research Institute, Amsterdam UMC, Amsterdam, the Netherlands
Department of Pediatric Endocrinology, Emma Children’s Hospital, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, the Netherlands

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Raoul Hennekam Department of Pediatrics, Emma Children’s Hospital, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands

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Eric Fliers Amsterdam Gastroenterology, Endocrinology & Metabolism (AGEM) Research Institute, Amsterdam UMC, Amsterdam, the Netherlands
Department of Endocrinology, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands

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Eveline Bruinstroop Amsterdam Gastroenterology, Endocrinology & Metabolism (AGEM) Research Institute, Amsterdam UMC, Amsterdam, the Netherlands
Department of Endocrinology, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands

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Anita Boelen Department of Laboratory Medicine, Endocrine Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands
Amsterdam Gastroenterology, Endocrinology & Metabolism (AGEM) Research Institute, Amsterdam UMC, Amsterdam, the Netherlands

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Tbl1xr1 Y446C/Y446C mice. However, circulating TH concentrations are not always consistent with tissue TH availability and action as, for example, seen in patients with resistance to thyroid hormone receptor-α (RTHα) ( 7 ). Two highly homologous

Article Type:
Research Article
Collections:
Thyroid hormone action
DOI:
https://doi.org/10.1530/ETJ-23-0077
Volume/Issue:
Volume 12: Issue 5
Open access
Yasmine Abdellaoui Department of Internal Medicine, Foch Hospital, Suresnes, France

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Dimitra Magkou Department of Endocrinology and Nutrition, Ambroise Paré Universitary Hospital, Assistance Publique Hôpitaux de Paris, Boulogne, France

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Sofia Bakopoulou Department of Endocrinology and Nutrition, Ambroise Paré Universitary Hospital, Assistance Publique Hôpitaux de Paris, Boulogne, France

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Ramona Zaharia Department of Endocrinology and Nutrition, Ambroise Paré Universitary Hospital, Assistance Publique Hôpitaux de Paris, Boulogne, France

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Marie-Laure Raffin-Sanson Department of Endocrinology and Nutrition, Ambroise Paré Universitary Hospital, Assistance Publique Hôpitaux de Paris, Boulogne, France
EA 4340, Université Versailles Saint Quentin en Yvelines, UFR Simone Veil Santé, Montigny le Bretonneux, France

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Laure Cazabat Department of Endocrinology and Nutrition, Ambroise Paré Universitary Hospital, Assistance Publique Hôpitaux de Paris, Boulogne, France
EA 4340, Université Versailles Saint Quentin en Yvelines, UFR Simone Veil Santé, Montigny le Bretonneux, France

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chemically intact TH [ 1 ]. The majority of these patients carry a mutation in the β isoform of the thyroid hormone receptor gene ( THRB ), which has an autosomal dominant transmission, a situation defined in the new nomenclature as resistance to thyroid

Article Type:
Case Report
DOI:
https://doi.org/10.1159/000506424
Volume/Issue:
Volume 9: Issue 5
Free access
Caiyan Mo Department of Endocrinology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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Han Chen Department of Endocrinology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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Qi Zhang Department of Endocrinology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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Ying Guo Department of Endocrinology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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Liyong Zhong Department of Endocrinology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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binding of thyroid-stimulating hormone receptor antibodies (TRAb) to thyroid-stimulating hormone (TSH) receptors leads to unregulated thyroid hormone production independent of pituitary TSH, resulting in hyperthyroidism ( 1 ). Central hyperthyroidism is a

Article Type:
Review Article
Collections:
Hyperthyroidism and thyrotoxicosis
DOI:
https://doi.org/10.1530/ETJ-22-0223
Volume/Issue:
Volume 12: Issue 4
Open access
Graham R. Williams Molecular Endocrinology Group, Department of Medicine, Imperial College London, London, UK

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intracellular T3 concentration and provide a pre-receptor control mechanism that regulates availability of the active hormone to the cell nucleus. Thyroid Hormone Receptors The thyroid hormone receptors TRα1, TRβ1 and TRβ2, bind ligand with high affinity

Article Type:
Review Article
DOI:
https://doi.org/10.1159/000345548
Volume/Issue:
Volume 2: Issue 1
Free access