Anti-Human TSHR (Clone M22) - Purified No Carrier Protein - 50 µg

All|Primary Monoclonal Antibodies

2 - 8°C Wet Ice

Graves’ disease is an autoimmune disease that can cause hyperthyroidism with TSH receptor (TSHR) autoantibodies (TRAbs) playing a key role in its pathogenesis1. There are two types of TRAbs, both of which inhibit thyroid-stimulating hormone (TSH) binding to its receptor TSHR: 1) stimulating TRAbs (TSHR agonists) which bind to the TSHR and mimic the biological activity of TSH by stimulating the cyclic AMP pathway and thyroid hormone synthesis and 2) blocking TRAbs (TSHR antagonists) which bind to the receptor but do not activate the cyclic AMP pathway. M22 is a thyroid-stimulating monoclonal antibody that was obtained from the peripheral blood lymphocytes of a 19-year-old male with Graves’ hyperthyroidism and type-1 diabetes mellitus1, 2, 3. M22 was generated by infecting lymphocytes with Epstein-Barr virus and fusing with mouse/human hybrid cell line K6H6/B52, 3. M22-TSHR crystal structure and mutation experiments have shown that M22 interacts with a number of TSHR residues, some of which affect the biological activity of M22 when mutated1. Additionally, structural analysis has shown that M22 pushes the extracellular domain of TSHR into an upright active conformation in amanner similar to its natural ligand TSH4.M22 strongly inhibits TSH binding to TSHR and is a potent thyroid stimulator (TSHR agonist), as determined by its ability to stimulate cyclic AMP production in Chinese hamster ovary cells2, 5. M22 can also act as an autoantibody to activate TSHR, causing abnormal production of thyroid hormones4. The utility of M22 in CAR-T cell therapy of thyroid cancer is being investigated6.

≥1.0 mg/ml

TSHR is primarily found on the surface of thyroid epithelial cells. TSHRcan also be found on adipose tissue, fibroblasts, the anterior pituitary gland, hypothalamus, andkidneys.