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Relevant bibliographies by topics / TSH receptor autoantibodies

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Academic literature on the topic 'TSH receptor autoantibodies'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "TSH receptor autoantibodies"

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Michalek, Krzysztof, Syed A. Morshed, Rauf Latif, and Terry F. Davies. "TSH receptor autoantibodies." Autoimmunity Reviews 9, no. 2 (2009): 113–16. http://dx.doi.org/10.1016/j.autrev.2009.03.012.

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Sanders, Jane, Yasuo Oda, Sara Roberts, et al. "The Interaction of TSH Receptor Autoantibodies with 125I-Labelled TSH Receptor." Journal of Clinical Endocrinology & Metabolism 84, no. 10 (1999): 3797–802. http://dx.doi.org/10.1210/jcem.84.10.6071.

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Abstract Detergent-solubilized porcine TSH receptor (TSHR) has been labeled with 125I using a monoclonal antibody to the C-terminal domain of the receptor. The ability of sera containing TSHR autoantibody to immunoprecipitate the labeled receptor was then investigated. Sera negative for TSHR autoantibody (as judged by assays based on inhibition of labeled TSH binding to detergent-solubilized porcine TSHR) immunoprecipitated about 4% of the labeled receptor, whereas sera with high levels of receptor autoantibody immunoprecipitated more than 25% of the labeled receptor. The ability to immunoprec

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Furmaniak, J., Y. Nakajima, F. A. Hashim, et al. "The TSH receptor: Structure and interaction with autoantibodies in thyroid disease." Acta Endocrinologica 116, no. 1_Suppl (1987): S157—S165. http://dx.doi.org/10.1530/acta.0.114s157.

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Abstract. Studies of the TSH receptor using affinity labelling with photoactive derivatives of TSH and analysis by SDS-PAGE have shown that the receptor contains 2 subunits (A and B), linked by a disulphide bridge. Similar results are obtained with TSH receptors from human, porcine and guinea pig thyroid tissue and from guinea pig fat. Analysis of affinity labelled receptors under non-denaturing conditions suggest that subunits additional to the A and B subunits are not present. Hydrodynamic measurements indicate that the receptor A subunit has an approximately spherical structure (Stokes' rad

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Zakarija, M., and J. M. McKenzie. "Autoantibodies to the TSH Receptor." Experimental and Clinical Endocrinology & Diabetes 97, no. 02/03 (2009): 165–69. http://dx.doi.org/10.1055/s-0029-1211057.

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Huang, G. C., K. S. Collison, A. M. McGregor, and J. P. Banga. "Expression of a human thyrotrophin receptor fragment in Escherichia coli and its interaction with the hormone and autoantibodies from patients with Graves' disease." Journal of Molecular Endocrinology 8, no. 2 (1992): 137–44. http://dx.doi.org/10.1677/jme.0.0080137.

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ABSTRACT Graves' disease is an autoimmune thyroid disease characterized by the presence of pathogenic autoantibodies to the TSH receptor (TSH-R). By using polymerase chain reaction, the extracellular region of the human TSH-R cDNA has been amplified and used to prepare recombinant TSH-R (extracellular) protein fused with glutathione-S-transferase (GST). Purification of the recombinant TSH-R (extracellular)-GST fusion protein was achieved by preparative gel electrophoresis in SDS or by preparative isoelectric focusing in urea. Following removal of SDS by detergent exchange or urea by dialysis,

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Furmaniak, J., J. Sanders, P. Sanders, J. Miller-Gallacher, M. M. Ryder, and B. Rees Smith. "Practical applications of studies on the TSH receptor and TSH receptor autoantibodies." Endocrine 68, no. 2 (2020): 261–64. http://dx.doi.org/10.1007/s12020-019-02180-9.

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Kakinuma, Ayumu, Gregorio D. Chazenbalk, Juan Carlos Jaume, Basil Rapoport, and Sandra M. McLachlan. "The Human Thyrotropin (TSH) Receptor in a TSH Binding Inhibition Assay for TSH Receptor Autoantibodies1." Journal of Clinical Endocrinology & Metabolism 82, no. 7 (1997): 2129–34. http://dx.doi.org/10.1210/jcem.82.7.4092.

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Seven years after the molecular cloning of the human TSH receptor (TSHR), the porcine TSHR remains in general use in the TSH binding inhibition (TBI) assay for autoantibodies to the TSHR. We compared porcine and recombinant human TSHR in two types of TBI assays: one using intact Chinese hamster ovary cells expressing the recombinant human TSHR on their surface, and the other using soluble receptors extracted from these cells with detergent. In the intact cell TBI assay, monolayers expressing large numbers of TSHR were less effective than cells expressing few receptors. These findings are consi

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Kakinuma, A. "The Human Thyrotropin (TSH) Receptor in a TSH Binding Inhibition Assay for TSH Receptor Autoantibodies." Journal of Clinical Endocrinology & Metabolism 82, no. 7 (1997): 2129–34. http://dx.doi.org/10.1210/jc.82.7.2129.

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Lytton, Simon D., and George J. Kahaly. "Bioassays for TSH-receptor autoantibodies: An update." Autoimmunity Reviews 10, no. 2 (2010): 116–22. http://dx.doi.org/10.1016/j.autrev.2010.08.018.

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Vlase, H., N. Matsuoka, P. N. Graves, R. P. Magnusson, and T. F. Davies. "Folding-Dependent Binding of Thyrotropin (TSH) and TSH Receptor Autoantibodies to the Murine TSH Receptor Ectodomain*." Endocrinology 138, no. 4 (1997): 1658–66. http://dx.doi.org/10.1210/endo.138.4.5037.

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Dissertations / Theses on the topic "TSH receptor autoantibodies"

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Hata, Misako. "Comparison of a novel cell-based reporter assay and a competitive binding ELISA for the detection of thyrotropin-receptor (TSHR) autoantibodies (TRAb) in Graves' disease patients." Ohio : Ohio University, 2010. http://www.ohiolink.edu/etd/view.cgi?ohiou1262099140.

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Book chapters on the topic "TSH receptor autoantibodies"

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Fenzi, G. F., P. Vitti, C. Marcocci, L. Chiovato, and E. Macchia. "TSH Receptor Autoantibodies Affecting Thyroid Cell Function." In Thyroid Autoimmunity. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0945-1_10.

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Tozzoli, Renato, and Nicola Bizzaro. "TSH receptor autoantibodies in Graves’ disease." In Translational Autoimmunity. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-12-824466-1.00013-3.

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Molnár, Ildikó. "Deiodinase Enzymes and Their Activities in Graves’ Hyperthyroidism." In Graves' Disease [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97007.

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The origin of hyperthyroidism in Graves’ disease was displayed demonstrating the complexity of the processes. The role of stimulating TSH receptor antibodies is the one factor for the production of increased thyroidal T3 and T4. The T3 and T4 formation in colloid-embedded thyroglobulin and the activities of thyroidal deiodinases [type 1 (DIO1) and type 2 (DIO2)] play a crucial role in that. The findings of different authors were summarized with respect to highlighting the role of tissue-specific deiodinase activities. Apart from the results of experimental studies, the clinical results were br

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Bakshi, Vasudha, and Gollapalli Rajeev Kumar. "Graves’ Disease." In Graves' Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97641.

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Graves’ disease (GD) is an autoimmune thyroid disorder where autoantibodies are produced against TSH (Thyroid Stimulating Hormone) receptor causing thyrotoxicosis. It is characterized by goiter, ophthalmopathy, and occasionally pretibial myxedema. The autoimmune mechanism causing disease is not well understood and it is complex. It involves multifactorial etiology involving environmental and genetic factors. Smoking and positive family history contributing to the development of GD. GD can be diagnosed based on the clinical manifestation and demonstrating low concentration of TSHs, high TRab (T

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Butler, Gary, and Jeremy Kirk. "Thyroid gland disorders." In Paediatric Endocrinology and Diabetes. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198786337.003.0009.

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• The thyroid gland produces all of the T<sub>4</sub> and 20% of T<sub>3</sub>. • Congenital hypothyroidism is caused by: ◦ anatomical defects: agenesis/dysgenesis, ectopic, sublingual ◦ inborn errors of thyroid hormone metabolism ◦ secondary (pituitary thyroid-stimulating hormone (TSH)) or tertiary (hypothalamic thyrotropin-releasing hormone) deficiency ◦ iodine deficiency (commonest cause worldwide of hypothyroidism, patients are usually euthyroid). • Genetic causes are rare. • In most countries worldwide, newborn TSH screening is performed at 0–5 days of age. Treatment with l-thyroxine is (

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Saran, Sanjay. "Graves’ Disease." In Graves' Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98686.

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Graves’ disease (GD) is an autoimmune disorder characterized by presence of TSH receptor autoantibody. It is most common cause of hyperthyroidism worldwide. Though GD can occur any age but peak incidence is seen during adulthood in between 20 to 50 years of age. GD is more commonly seen in female. GD is primarily disease of thyroid gland but affects multi organ system i.e. heart, liver, muscle, eye and skin. Symptoms and signs are result from hyperthyroidism or a consequence of underlying autoimmunity. Weight loss, fatigue, heat intolerance, tremor, and palpitations are the most common symptom

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S. Khan, Mosin, Suhail S. Lone, Sunia Faiz, Iqra Farooq, and Sabhiya Majid. "Graves’ Disease: Pathophysiology, Genetics and Management." In Graves' Disease [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98238.

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Graves’ disease is an autoimmune disorder in which hyperthyroidism (over active thyroid) is caused by the autoantibodies against the TSH receptor. It is mainly characterized by the appearance of goiter. The symptoms are wide ranging as thyroid hormone affects many body systems. It is common in women and in people with age below than 40. Graves’ disease is caused by a combination of genetic and environmental factors while genetics being the main cause. Graves’ disease is not a single gene defect but has a complex pattern of inheritance. Today it is clear that genetic predisposition to Graves’ d

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Nazmy Mwafy, Saleh, Wesam Mohammad Afana, and Asma’a Ali Hejaze. "Changes in Vitamin B₁₂, Iron, Thyroid Hormones, Thyroid Autoantibodies and Hematological Indices Levels in Patients Suffering from Helicobacter pylori Infection." In Helicobacter pylori Infection - An Up to Date on the Pathogenic Mechanisms, Diagnosis and Clinical Management [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108036.

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Helicobacter pylori infection has been recognized as a public health problem worldwide with raising prevalence in developing than the developed countries. More than 50% of the world’s population infected, and 80% of infected have no symptoms. Megaloblastic anemia can occur due to impaired DNA synthesis resulting from deficiencies of vitamin B12 and folate. The development of autoantibodies to thyroid peroxidase (anti-TPO), thyroglobulin (anti-Tg), and thyroid-stimulating hormone receptor (TSH-R) is the main characteristic of autoimmune thyroid disease. H. pylori may decrease absorption of oral

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Mittal, Madhukar, and Vanishri Ganakumar. "Graves Disease in Childhood." In Graves' Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97569.

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Graves’ disease (GD) is an autoimmune disease caused by autoantibodies against thyroid stimulating hormone receptor (TSH-R), resulting in stimulation of thyroid gland and overproduction of thyroid hormones resulting in clinical manifestations. It is uncommon in children and is 6 times more prevalent in females. The symptomatology, clinical and biochemical severity are a function of age of onset of disease. Prepubertal children tend to present with weight loss and bowel frequency, associated with accelerated growth and bone maturation. Older children are more likely to present with the classica

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Agrawal, Ruchi, and Shahnaz Ahmad. "Graves’ Disease: Novel Diagnostic Approaches and Emerging Treatment Options." In Graves' Disease - Diagnostic and Therapeutic Developments and New Therapeutic Horizons [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1007594.

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The fundamental pathophysiology of Graves’ hyperthyroidism involves the activation of the thyroid-stimulating hormone receptor [TSHR] by autoantibodies, resulting in excessive thyroid hormone secretion independent of the hypothalamic-pituitary-thyroid [HPT] axis and consequently leading to the clinical symptoms and signs of hyperthyroidism. Graves’ hyperthyroidism has been linked with significant morbidity and reduced quality of life. Over the past 70 years, the treatment options for Graves’ hyperthyroidism have remained unchanged and include antithyroid medications, radioiodine ablation, and

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