thyroid stimulating hormone receptor, ELISA Kit

Mouse Thyrotropin receptor (TSHR) ELISA kit; CHNG1; LGR3; MGC75129; hTSHR-I; seven transmembrane helix receptor; thyroid stimulating hormone receptor; isoform 2; thyrotropin receptor; thyrotropin receptor-I; hTSHR-I; thyroid stimulating hormone receptor

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

Store all reagents at 2-8 degree C

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Small volumes of TSHR elisa kit 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.

MBS9323783 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the thyroid stimulating hormone receptor (TSHR) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing TSHR. The ELISA analytical biochemical technique of the MBS9323783 kit is based on TSHR antibody-TSHR antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect TSHR antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, TSHR. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

86,583 Da

thyroid stimulating hormone receptor

thyrotropin receptor; TSH-R; thyroid-stimulating hormone receptor

Thyrotropin receptor

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TSHR_MOUSE

TSHR: 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). 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). Autoantibodies against TSHR are directly responsible for the pathogenesis and hyperthyroidism of Graves disease. Antibody interaction with TSHR results in an uncontrolled receptor stimulation. Defects in TSHR are the cause of congenital hypothyroidism non-goitrous type 1 (CHNG1); also known as congenital hypothyroidism due to TSH resistance. CHNG1 is 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. CHNG1 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. Defects in TSHR are the cause of familial gestational hyperthyroidism (HTFG). HTFG is a condition characterized by abnormally high levels of serum thyroid hormones occurring during early pregnancy. Defects in TSHR are the cause of hyperthyroidism non- autoimmune (HTNA). It is 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. Belongs to the G-protein coupled receptor 1 family. FSH/LSH/TSH subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral; Receptor, GPCR; Membrane protein, multi-pass; GPCR, family 1

Cellular Component: membrane; integral to membrane; plasma membrane; receptor complex; lipid raft

Molecular Function: G-protein coupled receptor activity; signal transducer activity; protein-hormone receptor activity; thyroid-stimulating hormone receptor activity

Biological Process: regulation of locomotion; G-protein coupled receptor protein signaling pathway; inner ear receptor stereocilium organization and biogenesis; ***** locomotory behavior; inner ear receptor cell development; B cell differentiation; positive regulation of cell proliferation; positive regulation of multicellular organism growth; signal transduction; G-protein signaling, adenylate cyclase activating pathway

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