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MCT8 and TSHR form heteromers.
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TSHR mutations occur in approximately 5% thyroid nodules in a large consecutive series with indeterminate cytology. TSHR mutations may be associated with an increased cancer risk when present at high allelic frequency
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This work is devoted to the ascertainment of serological cross-reactivity between OmpF porin from Yersinia pseudotuberculosis (YpOmpF) and human thyroid-stimulating hormone receptor (hTSHR).
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Genetic polymorphisms of CTLA-4 gene on the nucleotide 49 at codon 17 of exon 1, TSHR gene SNP rs2268458 of intron 1, number of regulatory T cells and TRAb levels play a role as risk factors for relapse in patients with Graves' disease.
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Overexpression of TSHR was found in a great majority of hepatocellular carcinomatissues and associated with unfavorable prognosis
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Signaling dissection using diverse inhibitors indicated that EOC cell proliferation driven by thyrostimulin-TSHR signaling is PKA independent, but does require the involvement of the MEK-ERK and PI3K-AKT signal cascades, which are activated mainly via the trans-activation of EGFR
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SNPs rs179247 and rs12101255 were significantly associated with Graves disease. rs12101255 and rs2268458 polymorphisms had no association with Graves diseases and Graves ophthalmopathy.
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Among the evaluated TSHR gene SNPs, the rs4411444 GG genotype and the rs4903961 C allele in the enhancer regions of the TSHR gene were most strongly associated with the development of Graves disease, especially intractable disease, and that of Hashimoto disease, respectively.
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Low expression of TSHR is associated with dilated cardiomyopathy and impaired left ventricular function accompanied by increased risk of death.
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Data suggest iodination of TG is involved in regulation of NIS expression in thyroid follicle via TSH/TSHR signaling; NIS expression and PKA activity are up-regulated by lowly iodinated TG; NIS expression is down-regulated and PKC activity up-regulated by highly iodinated TG. (TG, thyroglobulin; NIS, sodium/iodide symporter; PK, protein kinase; TSH, thyroid-stimulating hormone; TSHR, thyroid-stimulating hormone receptor)
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Monoallelic TSHR mutations are significantly associated with positive newborn screen for congenital hypothyroidism, and the association is further strengthened by the coexistence of monoallelic DUOX2 mutations.
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findings proved that iodinated TG in thyroid follicular lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways.
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The role of TSH Receptor cleavage into subunits and shedding of the A-Subunit in Graves' disease pathogenesis is reviewed.
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Data (including data from studies using knockout mice) suggest that thyrotropin/thyrotropin receptor signal transduction stimulates thyroglobulin phosphorylation and contributes to enhanced de novo triiodothyronine formation in thyrocytes.
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a hot-spot mutation in EZH1 is the second most frequent genetic alteration in autonomous thyroid adenomas; the association between EZH1 and TSHR mutations suggests a 2-hit model for the pathogenesis of these tumors, whereby constitutive activation of the cAMP pathway and EZH1 mutations cooperate to induce the hyperproliferation of thyroid cells
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Germline mutation in the thyrotropin receptor gene is associated with non-autoimmune hyperthyroidism.
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Congenital Hypothyroidism With Gland-in-Situ 59% attributable to mutations in TSHR.
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data support the association that low intrathymic TSHR expression is associated with susceptibility to developing pathogenic TSHR antibodies, while high intrathymic TSHR expression is protective
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Graves' disease is associated with polymorphisms of TSHR intron 1 rs179247 and rs12101255. There is no association between rs179247 SNPs and Graves' ophthalmopathy
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TSHR gene mutations p.R528C and c.392+4del4 associated with congenital hypothyroidism.
