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anti-Human TSH receptor Antibodies:
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Human Monoclonal TSH receptor Primary Antibody for FACS, IHC (p) - ABIN2476797
Costagliola, Rodien, Many, Ludgate, Vassart: Genetic immunization against the human thyrotropin receptor causes thyroiditis and allows production of monoclonal antibodies recognizing the native receptor. in Journal of immunology (Baltimore, Md. : 1950) 1998
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Cow (Bovine) Polyclonal TSH receptor Primary Antibody for WB - ABIN2777037
Claus, Jaeschke, Kleinau, Neumann, Krause, Paschke: A hydrophobic cluster in the center of the third extracellular loop is important for thyrotropin receptor signaling. in Endocrinology 2005
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Human Monoclonal TSH receptor Primary Antibody for IHC (p) - ABIN535220
Mizukami, Hashimoto, Nonomura, Michigishi, Nakamura, Noguchi, Matsukawa: Immunohistochemical demonstration of thyrotropin (TSH)-receptor in normal and diseased human thyroid tissues using monoclonal antibody against recombinant human TSH-receptor protein. in The Journal of clinical endocrinology and metabolism 1994
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Functional thyroid differentiation in zebrafish was examined and the role of TSHR signaling during thyroid organogenesis, was characterized.
MCT8 and TSHR form heteromers.
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
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).
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.
Overexpression of TSHR was found in a great majority of hepatocellular carcinomatissues and associated with unfavorable prognosis
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
SNPs rs179247 and rs12101255 were significantly associated with Graves disease. rs12101255 and rs2268458 polymorphisms had no association with Graves diseases and Graves ophthalmopathy.
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.
Low expression of TSHR is associated with dilated cardiomyopathy and impaired left ventricular function accompanied by increased risk of death.
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)
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.
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.
The role of TSH Receptor cleavage into subunits and shedding of the A-Subunit in Graves' disease pathogenesis is reviewed.
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.
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
Germline mutation in the thyrotropin receptor gene is associated with non-autoimmune hyperthyroidism.
Congenital Hypothyroidism With Gland-in-Situ 59% attributable to mutations in TSHR.
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
Graves' disease is associated with polymorphisms of TSHR intron 1 rs179247 and rs12101255. There is no association between rs179247 SNPs and Graves' ophthalmopathy
TSHR gene mutations p.R528C and c.392+4del4 associated with congenital hypothyroidism.
Data suggest that stimulation of Tsh/Tshr signaling increases apoptosis and suppresses autophagy in primary chondrocytes.
Unlike its critical role in maintaining the normal growth and function of the thyroid gland, our results demonstrated that hepatic TSHR is involved in liver lipid metabolism and has little effect on energy metabolism.
Data indicate that splenic T cells from thyroid stimulating hormone receptor (TSHR) A-subunit primed animals undergoing Graves' orbitopathy (GO) showed proliferative responses to purified TSHR antigen and secreted proinflammatory cytokines.
Lung fibroblasts of TSHR KO mice have decreased cell surface Igf1r expression, and have Igf1r protein and protein fragments in both cytoplasm and nucleus. Igf1r mRNA levels were similar between TSHR KO and WT mice.
The mechanism, underlying TSH-induced liver triglyceride accumulation, involved that TSH, through its receptor TSHR, triggered hepatic SREBP-1c activity.
These findings suggest that activation of TSHR directly inhibits FASN expression in mature adipocytes, possibly mediated by PKA and ERK
A novel role for TSHR in behavioral and neurological phenotypes of Attention deficit/hyperactivity disorder.
The data indicate functional TSHR is expressed in ventricular myocytes and mediates TSH-induced BNP secretion and HMGCR up-regulation through the cAMP/PKA/pCREB signaling pathway.
findings demonstrate TSH-R expression is thymus-specific within the immune system; data support the notion of a novel neuroendocrine-immune interaction in which TSH-R signaling in the thymus, most likely mediated by TSH, enhances thymic T-cell development
The inhibition of hepatic PEPCK and G6P and enhanced expression of GK contributed to the development of fasting hypoglycemia in Tshr-ko mice.
UCP-1 and TSHR co-localized in retrobulbar adipose tissues in murine models of Graves' disease.
Cloned a thyroid-stimulating hormone receptor (TSHR) cDNA from thyroid glands. The sequence of this cDNA indicated that it encoded a 739 amino acid TSHR splice variant that lacked exon 5 (TSHR739).
Data indicate that osteoporosis due to thyroid stimulating hormone receptor Tshr deficiency, at least in part, arises from elevated Tnfalpha expression.
Study with mouse monoclonal antibody 3BD10 confirms TSHR conformational heterogeneity and suggests that the N-terminal cysteine cluster may contribute to this structural variability.
Messenger RNA levels of hormone-sensitive lipase in epididymal fat containing the transferred TSHR gene were twofold higher than those in tissue from the control side
Thyroid hormone receptors control developmental maturation of the middle ear and the size of the ossicular bones
thyroid-stimulating hormone and thyroid-stimulating hormone receptor antibodies have roles in osteoclastogenesis
Data demonstrate the key role of TSH signaling in Braf-induced papillary thyroid cancer initiation and provide experimental support for observations in humans pointing to a strong association between TSH levels and thyroid cancer incidence.
Studies indicate it is important to refine knowledge and insights in non-autoimmune diseases caused by defects of the TSHR gene and it might help to develop pharmacological means for compensation of uncontrolled thyroid growth.
TSHR KO mice are, therefore, of value for future studies dissecting the autoimmune response to the mouse TSHR.
Localization of thyrotropin receptor and thyroglobulin in the bovine corpus luteum.
analysis of activation switch in the thyrotropin receptor
Rhes can interfere with the functional activity of wt and mutated TSHr.
Increased receptor binding by bovine (b) TSH bound to monoclonal antibody to bTSHbeta-subunit.
the hinge region represents an extracellular intermediate connector for both hormone binding and signal transduction of the thyroid stimulating hormone receptor
The equine TSHR is not responsive to equine chorionic gonadotropin but is more sensitive to human CG than the human TSHR
The protein encoded by this gene is a membrane protein and a major controller of thyroid cell metabolism. The encoded protein is a receptor for thyrothropin and thyrostimulin, and its activity is mediated by adenylate cyclase. Defects in this gene are a cause of several types of hyperthyroidism. Three transcript variants encoding different isoforms have been found for this gene.
, thyroid-stimulating hormone receptor
, thyrotropin receptor
, seven transmembrane helix receptor
, thyrotropin receptor-I, hTSHR-I