Mouse Regulator Of G Protein Signaling 5 (RGS5) ELISA Kit-Sandwich

Regulator of G-protein signaling 5 (RGS5) inhibits signal transduction by increasing the GTPase activity of G-protein alpha subunits, thereby converting them to their inactive GDP-bound state. It binds specifically to G(i)-alpha and G(o)-alpha, but not G(s)-alpha. In mice, RGS5 has extensive and complex functions, including roles in vascular development, cardiac function, neuroinflammation, metabolic regulation, and blood pressure control. A deficiency in RGS5 leads to delayed atrial repolarization, prolonged action potential duration, and a higher incidence of atrial fibrillation. In mouse models induced with LPS, the absence of RGS5 significantly reduces the expression of inflammatory factors (such as TNFα) and mitigates the degeneration of dopamine neurons. This suggests that RGS5 plays a protective role in neuroinflammatory and neurodegenerative diseases.