Thyrotropin receptor, Thyroid-stimulating hormone receptor, TSH-R, TSHR, LGR3

For Research Use Only. Not for use in diagnostic procedures.

Chromosome: 14; NC_000014.8 (81421333..81612646). Location: 14q31

>90% by SDS-PAGE

Liquid (2.5 mg/ml); Each vial contains 8M Urea,Tris-HCl (pH7.4 ±0.2),with 0.02% NaN₃.

Ships in blue ice.
Upon receipt, aliquot and store at -20°C or -80°C for long term.
Avoid repeated freeze and thaw cycles.

Small volumes of TSHR recombinant protein vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Background/Introduction: Thyroid stimulating hormone receptor (TSHR), also known as Thyrotropin receptor is a member of the leucine-rich repeat-containing G protein-coupled receptors. G protein-coupled receptors (GPCRs) are the largest family of plasma membrane receptors. They mediate the effects of several endogenous cues and serve as important pharmacological targets. TSHR is primarily found on the surface of the thyroid epithelial cells. Both TSHR and its ligand TSH have evolved to acquire specificity, minimize cross-reaction to other glycoprotein hormone receptors, and modulate cognate interaction (and thereby thyrotropic activity).

ELISA (EIA), SDS-PAGE

Other applications have not been tested. The optimal dilutions should be determined by end user.

thyroid stimulating hormone receptor

thyrotropin receptor; thyrotropin receptor-I, hTSHR-I; seven transmembrane helix receptor; thyroid stimulating hormone receptor, isoform 2

Thyrotropin receptor

LGR3; TSH-R??[Similar Products]

TSHR_HUMAN

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. [provided by RefSeq, Dec 2008]

Function: Receptor for thyrothropin. Plays a central role in controlling thyroid cell metabolism. The activity of this receptor is mediated by G proteins which activate adenylate cyclase. Also acts as a receptor for thyrostimulin (GPA2+GPB5). Ref.11

Subunit structure: Interacts (via the PDZ-binding motif) with SCRIB; regulates TSHR trafficking and function. Ref.11 Ref.12

Subcellular location: Cell membrane; Multi-pass membrane protein.

Tissue specificity: Expressed in the thyroid. Ref.2

Polymorphism: The Asp727Glu polymorphism is associated with Graves disease in a Russian population. The Glu727 allele and the heterozygous Asp727Glu genotype are related to higher risk of the disease. The Asp727Glu polymorphism significantly ameliorates G(s)alpha protein activation in the presence of the gain-of-function mutation Ala593Asn although it is functionally inert in the context of the wild-type TSHR.

Involvement in disease: Defects in TSHR are found in patients affected by hyperthyroidism with different etiologies. Somatic, constitutively activating TSHR mutations and/or constitutively activating G(s)alpha mutations have been identified in toxic thyroid nodules (TTNs) that are the predominant cause of hyperthyroidism in iodine deficient areas. These mutations lead to TSH independent activation of the cAMP cascade resulting in thyroid growth and hormone production. TSHR mutations are found in autonomously functioning thyroid nodules (AFTN), toxic multinodular goiter (TMNG) and hyperfunctioning thyroid adenomas (HTA). TMNG encompasses a spectrum of different clinical entities, ranging from a single hyperfunctioning nodule within an enlarged thyroid, to multiple hyperfunctioning areas scattered throughout the gland. HTA are discrete encapsulated neoplasms characterized by TSH-independent autonomous growth, hypersecretion of thyroid hormones, and TSH suppression. Defects in TSHR are also a cause of thyroid neoplasms (papillary and follicular cancers). Ref.15 Ref.16 Ref.17Autoantibodies against TSHR are directly responsible for the pathogenesis and hyperthyroidism of Graves disease. Antibody interaction with TSHR results in an uncontrolled receptor stimulation. Ref.15 Ref.16 Ref.17Hypothyroidism, congenital, non-goitrous, 1 (CHNG1) [MIM:275200]: A non-autoimmune condition characterized by resistance to thyroid-stimulating hormone (TSH) leading to increased levels of plasma TSH and low levels of thyroid hormone. It presents variable severity depending on the completeness of the defect. Most patients are euthyroid and asymptomatic, with a normal sized thyroid gland. Only a subset of patients develop hypothyroidism and present a hypoplastic thyroid gland.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.15 Ref.16 Ref.17 Ref.27 Ref.32 Ref.34 Ref.36 Ref.39 Ref.50 Ref.53 Ref.61 Ref.63 Ref.67 Ref.69Familial gestational hyperthyroidism (HTFG) [MIM:603373]: A condition characterized by abnormally high levels of serum thyroid hormones occurring during early pregnancy.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.15 Ref.16 Ref.17 Ref.43Hyperthyroidism, non-autoimmune (HTNA) [MIM:609152]: A condition characterized by abnormally high levels of serum thyroid hormones, thyroid hyperplasia, goiter and lack of anti-thyroid antibodies. Typical features of Graves disease such as exophthalmia, myxedema, antibodies anti-TSH receptor and lymphocytic infiltration of the thyroid gland are absent.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.15 Ref.16 Ref.17 Ref.24 Ref.26 Ref.30 Ref.31 Ref.37 Ref.38 Ref.41 Ref.42 Ref.44 Ref.51 Ref.54 Ref.55 Ref.57 Ref.58 Ref.59 Ref.68

Sequence similarities: Belongs to the G-protein coupled receptor 1 family. FSH/LSH/TSH subfamily.Contains 7 LRR (leucine-rich) repeats.

Sequence caution: The sequence AAA70232.1 differs from that shown. Reason: Frameshift at positions 130, 135 and 612.

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