Thyroid Stimulating Hormone Receptor (TSHR)

The TSH receptor is a member of the G protein-coupled receptor superfamily of
integral membrane proteins.

The thyrotropin receptor (or TSH receptor) locates primarily in the body of the
thyroid gland. It recognizes and binds to stimulating thyroid hormone (also
known as "thyrotropin") secreted from the pituitary gland.

TSH stimulates the production of thyroxine (T4) and triiodothyronine (T3).

TSHR is closely related to the pathogenesis of various autoimmune thyroid
diseases and is an essential indicator for the clinical diagnosis of these
diseases.

SEKBIO is now offering Mouse anti-human TSHR mAb, Humanized anti-human TSHR
mAb, Recombinant human sTSHR (Soluble), and human TSHR extractive of cell
membranes (Full length) for diagnosis usage.

TSHR
Thyroid-stimulating hormone receptor (TSHR) and its homologous luteinizing
hormone/chorionic gonadotropin receptor and follicle-stimulating hormone
receptor belong to a class of glycoprotein receptors. They are also visual A
member of the large family of G protein-coupled receptors (GPcRs) of rhodopsin
(approximately 45% identity at the amino acid level). TSHR is mainly expressed
in thyroid follicular cells and activates the protein kinase A (PKA) and
phospholipase C (Phospholipases C, PLc) signal transduction systems after
combining with thyroid-stimulating hormone (TSH) under physiological
conditions. , regulate the growth and differentiation of the thyroid, and
promote the synthesis and release of thyroid hormones.

Anti TSH Antibody
The expression of TSHR can also be found in other cells or tissues, including
adipocytes, fibroblasts, osteoblasts and osteoclasts, bone marrow cells and
cardiomyocytes, etc., and is expressed in embryonic stem cells at an early
stage. In autoimmune thyroid diseases, especially toxic diffuse goiter (Graves'
disease, GD), TSHR can act as an autoantigen and bind to thyroid-stimulating
antibody (TSAb) to produce TSH-like stimulation. The reaction will eventually
lead to the loss of thyroid autoimmune tolerance, production and release of
excessive thyroid hormones, and clinical manifestations of hyperthyroidism such
as palpitations, sweating, and hyperthyroidism. Therefore, studying the
structure of thyroid-stimulating hormone receptors and elucidating the
interaction between autoantibodies and thyroid-stimulating hormone receptor
(TSHR) molecules is vital for understanding Graves disease's pathogenesis, a
common organ-specific autoimmune disease, and guiding clinical practice.
Diagnosis and treatment have far-reaching significance.

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