Associated Papers
Comparative genomic and clinicopathological analysis uncovers contrasting molecular profiles of canine and human thyroid carcinomas.
Das S et al.
Communications Biology, 2025
A de novo pathogenic variant in TSHR expanding the phenotype of persistent sporadic congenital non-autoimmune hyperthyroidism: a case report and literature review.
Xu W et al.
Translational Pediatrics, 2025
Genotype-Phenotype Correlation in Germline TSH Receptor Activating Mutation Associated Hyperthyroidism: A Systematic Review.
Yamichannaiah C et al.
Clinical Endocrinology, 2025
Delayed Presentation With Atypical Extrathyroidal Manifestations of Sporadic Non-autoimmune Congenital Hyperthyroidism: A Case Report and Literature Review.
Dighe R et al.
Cureus, 2025
TSHRV656F Activating Variant of the Thyroid Stimulating Hormone Receptor Gene in Neonatal Onset Hyperthyroidism: A Case Review
Kayaş L et al.
Journal of Clinical Research in Pediatric Endocrinology, 2022
Sensitive Sequencing Analysis Suggests Thyrotropin Receptor and Guanine Nucleotide-Binding Protein G Subunit Alpha as Sole Driver Mutations in Hot Thyroid Nodules.
Stephenson A et al.
Thyroid : Official Journal of the American Thyroid Association, 2020
Thyrotropin Receptor: Allosteric Modulators Illuminate Intramolecular Signaling Mechanisms at the Interface of Ecto- and Transmembrane Domain.
Marcinkowski P et al.
Molecular Pharmacology, 2019
How genetic errors in GPCRs affect their function: Possible therapeutic strategies.
Stoy H et al.
Genes & Diseases, 2015
Somatic mutations in 33 benign and malignant hot thyroid nodules in children and adolescents.
Eszlinger M et al.
Molecular and Cellular Endocrinology, 2014
Assessment of computational methods for predicting the effects of missense mutations in human cancers.
Gnad F et al.
Bmc Genomics, 2013
The hinge region of human thyroid-stimulating hormone (TSH) receptor operates as a tunable switch between hormone binding and receptor activation.
Majumdar R et al.
Plos One, 2012
The hinge region of the TSH receptor stabilizes ligand binding and determines different signaling profiles of human and bovine TSH.
Jaeschke H et al.
Endocrinology, 2011
Molecular description of non-autoimmune hyperthyroidism at a neonate caused by a new thyrotropin receptor germline mutation.
Biebermann H et al.
Thyroid Research, 2011
Shared sporadic and somatic thyrotropin receptor mutations display more active in vitro activities than familial thyrotropin receptor mutations.
Lueblinghoff J et al.
Thyroid : Official Journal of the American Thyroid Association, 2011
Genetic defects, thyroid growth and malfunctions of the TSHR in pediatric patients.
Biebermann H et al.
Frontiers in Bioscience (landmark Edition), 2010
Identification and evaluation of constitutively active thyroid stimulating hormone receptor mutations.
Lado-Abeal J et al.
Methods in Enzymology, 2010
Cases of borderline in vitro constitutive thyrotropin receptor activity: how to decide whether a thyrotropin receptor mutation is constitutively active or not?
Mueller S et al.
Thyroid : Official Journal of the American Thyroid Association, 2009
Prevalence of mutations in TSHR, GNAS, PRKAR1A and RAS genes in a large series of toxic thyroid adenomas from Galicia, an iodine-deficient area in NW Spain.
Palos-Paz F et al.
European Journal of Endocrinology, 2008
Constitutive activation of G protein-coupled receptors and diseases: insights into mechanisms of activation and therapeutics.
Tao YX
Pharmacology & Therapeutics, 2008
Molecular and structural effects of inverse agonistic mutations on signaling of the thyrotropin receptor--a basally active GPCR.
Kleinau G et al.
Cellular and Molecular Life Sciences : Cmls, 2008
Evidence for cooperative signal triggering at the extracellular loops of the TSH receptor.
Kleinau G et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2008
The thyrotropin receptor hinge region is not simply a scaffold for the leucine-rich domain but contributes to ligand binding and signal transduction.
Mizutori Y et al.
Molecular Endocrinology (baltimore, Md.), 2008
Suppression of thyrotropin receptor constitutive activity by a monoclonal antibody with inverse agonist activity.
Chen CR et al.
Endocrinology, 2007
Contacts between extracellular loop two and transmembrane helix six determine basal activity of the thyroid-stimulating hormone receptor.
Kleinau G et al.
The Journal of Biological Chemistry, 2007
Similar prevalence of somatic TSH receptor and Gsalpha mutations in toxic thyroid nodules in geographical regions with different iodine supply in Turkey.
Gozu HI et al.
European Journal of Endocrinology, 2006
A hydrophobic cluster in the center of the third extracellular loop is important for thyrotropin receptor signaling.
Claus M et al.
Endocrinology, 2005
Interactions between the extracellular domain and the extracellular loops as well as the 6th transmembrane domain are necessary for TSH receptor activation.
Neumann S et al.
European Journal of Endocrinology, 2005
Biological activity of activating thyroid-stimulating hormone receptor mutants depends on the cellular context.
Fuhrer D et al.
Endocrinology, 2003
Expression of G(alpha)(s) proteins and TSH receptor signalling in hyperfunctioning thyroid nodules with TSH receptor mutations.
Holzapfel HP et al.
European Journal of Endocrinology, 2002
Thyrotropin receptor mutations as a tool to understand thyrotropin receptor action.
Wonerow P et al.
Journal of Molecular Medicine (berlin, Germany), 2001
Functional characterization of five constitutively activating thyrotrophin receptor mutations.
Wonerow P et al.
Clinical Endocrinology, 2000
The extracellular thyrotropin receptor domain is not a major candidate for mutations in toxic thyroid nodules.
Führer D et al.
Thyroid : Official Journal of the American Thyroid Association, 1998
[Disorders caused by mutations of the thyrotropin receptor].
Kosugi S
Nihon Rinsho. Japanese Journal of Clinical Medicine, 1998
Somatic mutations in the thyrotropin receptor gene and not in the Gs alpha protein gene in 31 toxic thyroid nodules.
Führer D et al.
The Journal of Clinical Endocrinology and Metabolism, 1997