Recombinant Human NPR-C protein

Supplementary information

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

The NPR-C also known as natriuretic peptide receptor C functions as an important regulator in the homeostasis of cardiovascular and renal functions. It is also referred to as atrial natriuretic peptide receptor C (ANPRC). This protein does not possess guanylyl cyclase activity unlike its counterparts NPR-A and NPR-B but instead acts via clearance binding of natriuretic peptides preventing them from binding to other receptors. The receptor has a molecular mass of approximately 60 kDa and is widely expressed in tissues such as vascular endothelium kidney and adipose tissue.

Biological function summary

NPR-C binds multiple natriuretic peptides including ANP BNP and CNP and modulates their effects by facilitating their clearance from circulation. This receptor does not function as part of a larger protein complex unlike other receptor subtypes. It controls blood volume and pressure by influencing the natriuretic diuretic and vasorelaxant actions of its peptide ligands. NPR-C helps maintain fluid balances and prevents overactivation of hormonal pathways linked to cardiovascular conditions.

Pathways

NPR-C serves an important role in the natriuretic peptide signaling pathway primarily through the regulation of peptide availability. It physically interacts with several circulating natriuretic peptides but not through second messenger cascades. NPR-C is integral to maintaining the balance between the ANP receptor pathway and the renin-angiotensin-aldosterone system therefore indirectly modulating the functions of NPR-A and NPR-B which are responsible for cyclic GMP-dependent signaling.

NPR-C contributes to the pathophysiology of hypertension and heart failure by overseeing the peptide-hormone balance in the cardiovascular system. Anomalies in NPR-C expression or function can lead to improper regulation of blood pressure and fluid retention. Its interaction with proteins such as angiotensin II receptors can exacerbate the effects of hypertension. Understanding the role of NPR-C in these conditions presents potential therapeutic targets for modulating cardiovascular diseases.