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Relevant bibliographies by topics / Thyroid stimulation hormone receptor (TSHR)

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Journal articles

Academic literature on the topic 'Thyroid stimulation hormone receptor (TSHR)'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Thyroid stimulation hormone receptor (TSHR)"

1

Szkudlinski, Mariusz W., Valerie Fremont, Catherine Ronin, and Bruce D. Weintraub. "Thyroid-Stimulating Hormone and Thyroid-Stimulating Hormone Receptor Structure-Function Relationships." Physiological Reviews 82, no. 2 (2002): 473–502. http://dx.doi.org/10.1152/physrev.00031.2001.

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This review focuses on recent advances in the structure-function relationships of thyroid-stimulating hormone (TSH) and its receptor. TSH is a member of the glycoprotein hormone family constituting a subset of the cystine-knot growth factor superfamily. TSH is produced by the pituitary thyrotrophs and released to the circulation in a pulsatile manner. It stimulates thyroid functions using specific membrane TSH receptor (TSHR) that belongs to the superfamily of G protein-coupled receptors (GPCRs). New insights into the structure-function relationships of TSH permitted better understanding of th

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2

Neumann, Susanne, Wenwei Huang, Elena Eliseeva, Steve Titus, Craig J. Thomas, and Marvin C. Gershengorn. "A Small Molecule Inverse Agonist for the Human Thyroid-Stimulating Hormone Receptor." Endocrinology 151, no. 7 (2010): 3454–59. http://dx.doi.org/10.1210/en.2010-0199.

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Small molecule inverse agonists for the TSH receptor (TSHR) may be used as probes of the role of basal (or agonist-independent or constitutive) signaling and may have therapeutic potential as orally active drugs to inhibit basal signaling in patients with thyroid cancer and in some patients with hyperthyroidism. We describe the first small-molecule ligand [1;2-(3-((2,6-dimethylphenoxy)methyl)-4-methoxyphenyl)-3-(furan-2-ylmethyl)-2,3-dihydroquinazolin-4(1H)-one] that exhibits inverse agonist properties at TSHR. 1 inhibits basal and TSH-stimulated signaling, measured as cAMP production, by TSHR

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3

Decroli, Eva, and Alexander Kam. "Dampak Klinis Thyroid-Stimulating Hormone." Jurnal Kesehatan Andalas 6, no. 1 (2017): 222. http://dx.doi.org/10.25077/jka.v6i1.674.

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Thyroid-Stimulating Hormone (TSH), yang disebut juga dengan tirotropin, adalah glikoprotein yang disekresikan oleh bagian anterior dari kelenjar hipofisis. Sintesis dan sekresi dari TSH diatur oleh faktor dari hipotalamus yang didominasi oleh thyrotropin-releasing hormone (TRH) dan faktor perifer yang didominasi oleh kadar hormon tiroid. Setelah disintesis, TSH disekresikan, lalu akan berikatan dengan reseptor yang disebut Thyroid-Stimulating Hormone Receptor (TSHR). Ikatan TSH-TSHR akan memberikan dampak klinis terhadap jaringan dan organ tempat terjadinya ikatan tersebut. Ikatan tersebut bis

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4

Neumann, Susanne, Wenwei Huang, Elena Eliseeva, Steve Titus, Craig J. Thomas, and Marvin C. Gershengorn. "A Small Molecule Inverse Agonist for the Human Thyroid-Stimulating Hormone Receptor." Endocrine Reviews 31, no. 3 (2010): 403. http://dx.doi.org/10.1210/edrv.31.3.9992.

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ABSTRACT Small molecule inverse agonists for the TSH receptor (TSHR) may be used as probes of the role of basal (or agonist-independent or constitutive) signaling and may have therapeutic potential as orally active drugs to inhibit basal signaling in patients with thyroid cancer and in some patients with hyperthyroidism. We describe the first small-molecule ligand [1, 2-(3-((2,6-dimethylphenoxy)methyl)-4-methoxyphenyl)-3-(furan-2-ylmethyl)-2,3-dihydroquinazolin-4(1H)-one] that exhibits inverse agonist properties at TSHR. 1 inhibits basal and TSH-stimulated signaling, measured as cAMP productio

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5

Ando, Takao, and Terry F. Davies. "Monoclonal Antibodies to the Thyrotropin Receptor." Clinical and Developmental Immunology 12, no. 2 (2005): 137–43. http://dx.doi.org/10.1080/17402520500078238.

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The thyrotropin receptor (TSHR) is a seven transmembrane G-protein linked glycoprotein expressed on the thyroid cell surface and which, under the regulation of TSH, controls the production and secretion of thyroid hormone from the thyroid gland. This membrane protein is also a major target antigen in the autoimmune thyroid diseases. In Graves' disease, autoantibodies to the TSHR (TSHR-Abs) stimulate the TSHR to produce thyroid hormone excessively. In autoimmune thyroid failure, some patients exhibit TSHR-Abs which block TSH action on the receptor. There have been many attempts to generate huma

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6

Neumann, Susanne, Christine C. Krieger, and Marvin C. Gershengorn. "Targeting TSH and IGF-1 Receptors to Treat Thyroid Eye Disease." European Thyroid Journal 9, Suppl. 1 (2020): 59–65. http://dx.doi.org/10.1159/000511538.

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Graves’ disease (GD) is an autoimmune disease caused in part by thyroid-stimulating antibodies (TSAbs) that activate the thyroid-stimulating hormone receptor (TSHR). In Graves’ hyperthyroidism (GH), TSAbs cause persistent stimulation of thyroid cells leading to continuous thyroid hormone synthesis and secretion. Thyroid eye disease (TED), also called Graves’ orbitopathy, is an orbital manifestation of GD. We review the important roles of the TSHR and the insulin-like growth factor 1 receptor (IGF-1R) in the pathogenesis of TED and discuss a model of TSHR/IGF-1R crosstalk that considers two pat

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7

Holthoff, Hans-Peter, Kerstin Uhland, Gabor Laszlo Kovacs, et al. "Thyroid-stimulating hormone receptor (TSHR) fusion proteins in Graves’ disease." Journal of Endocrinology 246, no. 2 (2020): 135–47. http://dx.doi.org/10.1530/joe-20-0061.

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Graves’ disease is an autoimmune disorder, which is characterized by stimulatory antibodies targeting the human thyrotropin receptor (TSHR), resulting in hyperthyroidism and multiple organ damage. We systematically investigated monomeric and dimeric fusion proteins of the A subunit of TSHR for efficacy to bind to the monoclonal patient antibody M22, to interact with Graves’ patient serum samples, and to impact on anti-TSHR antibody titers, hyperthyroidism, tachycardia and other in vivo read-outs in a long-term mouse model of Graves’ disease induced by immunization with a recombinant adenovirus

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8

Rowe, Christopher W., Jonathan W. Paul, Craig Gedye, et al. "Targeting the TSH receptor in thyroid cancer." Endocrine-Related Cancer 24, no. 6 (2017): R191—R202. http://dx.doi.org/10.1530/erc-17-0010.

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Recent advances in the arena of theranostics have necessitated a re-examining of previously established fields. The existing paradigm of therapeutic thyroid-stimulating hormone receptor (TSHR) targeting in the post-surgical management of differentiated thyroid cancer using levothyroxine and recombinant human thyroid-stimulating hormone (TSH) is well understood. However, in an era of personalized medicine, and with an increasing awareness of the risk profile of longstanding pharmacological hyperthyroidism, it is imperative clinicians understand the molecular basis and magnitude of benefit for i

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9

Chu, Yu-De, and Chau-Ting Yeh. "The Molecular Function and Clinical Role of Thyroid Stimulating Hormone Receptor in Cancer Cells." Cells 9, no. 7 (2020): 1730. http://dx.doi.org/10.3390/cells9071730.

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The thyroid stimulating hormone (TSH) and its cognate receptor (TSHR) are of crucial importance for thyrocytes to proliferate and exert their functions. Although TSHR is predominantly expressed in thyrocytes, several studies have revealed that functional TSHR can also be detected in many extra-thyroid tissues, such as primary ovarian and hepatic tissues as well as their corresponding malignancies. Recent advances in cancer biology further raise the possibility of utilizing TSH and/or TSHR as a therapeutic target or as an informative index to predict treatment responses in cancer patients. The

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10

Núñez Miguel, R., J. Sanders, D. Y. Chirgadze, T. L. Blundell, J. Furmaniak, and B. Rees Smith. "FSH and TSH binding to their respective receptors: similarities, differences and implication for glycoprotein hormone specificity." Journal of Molecular Endocrinology 41, no. 3 (2008): 145–64. http://dx.doi.org/10.1677/jme-08-0040.

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The crystal structures of the leucine-rich repeat domain (LRD) of the FSH receptor (FSHR) in complex with FSH and the TSH receptor (TSHR) LRD in complex with the thyroid-stimulating autoantibody (M22) provide opportunities to assess the molecular basis of the specificity of glycoprotein hormone–receptor binding. A comparative model of the TSH–TSHR complex was built using the two solved crystal structures and verified using studies on receptor affinity and activation. Analysis of the FSH–FSHR and TSH–TSHR complexes allowed identification of receptor residues that may be important in hormone-bin

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