Anti-TSH Receptor/TSH-R antibody [SPM223]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The TSH Receptor (TSH-R) also known as thyrotropin receptor is an important protein in the regulation of the thyroid gland. Its molecular mass is approximately 84 kDa. TSH-R is predominantly expressed on the surface of thyroid follicular cells. This receptor functions mechanically by binding thyroid-stimulating hormone (TSH) initiating a cascade that increases the production and release of thyroid hormones such as thyroxine (T4) and triiodothyronine (T3). This receptor is critical in maintaining proper thyroid function.

Biological function summary

TSH-R plays an important role in the regulation of metabolic processes. As part of the endocrine system the TSH-R interacts with TSH secreted by the anterior pituitary modulating signaling pathways that contribute to cell growth differentiation and hormone production in the thyroid gland. TSH-R is a component of the G protein-coupled receptor family sharing structural similarities with other receptors in this group. Additionally its activation influences the synthesis of both T4 and T3 which are essential for normal development metabolism and thermoregulation.

Pathways

The TSH-R is important in the cyclic AMP (cAMP) signaling pathway. Upon TSH binding the receptor activates adenylate cyclase via the Gs protein resulting in cAMP production. This activation influences several downstream processes that promote thyroid hormone synthesis and secretion. Furthermore TSH-R engages in cross-talk with other pathways related to cell proliferation and survival. The receptor is linked with proteins like G proteins that mediate its signaling effects integrating into the broader network of hormonal regulation.

Associated diseases and disorders

TSH-R is strongly associated with autoimmune thyroid diseases particularly Graves' disease and Hashimoto's thyroiditis. In Graves’ disease stimulating antibodies known as thyroid-stimulating immunoglobulins (TSI) mimic TSH and activate the TSH-R causing overproduction of thyroid hormones and leading to hyperthyroidism. In Hashimoto's thyroiditis TSH-R participates indirectly as autoantibodies can lead to receptor destruction and subsequent hypothyroidism. These conditions often involve interactions with additional immune-related proteins such as T cells and cytokines affecting overall immune tolerance in the thyroid gland.