Rat Atrial Natriuretic Peptide Receptor 2 (NPR2) Protein

Background

NPR2, also known as guanylyl cyclase-B, primarily binds C-type natriuretic peptide (CNP), a critical regulator of skeletal growth and bone homeostasis. Similar to NPR1, NPR2 activation leads to cGMP production, which modulates cellular processes such as chondrocyte proliferation, bone elongation, and vascular relaxation. NPR2 is highly expressed in growth plate chondrocytes, vascular smooth muscle cells, and the nervous system. Loss-of-function mutations in NPR2 are associated with skeletal dysplasias, such as acromesomelic dysplasia type Maroteaux, characterized by short stature and abnormal bone growth. In the vascular system, NPR2-mediated CNP signaling contributes to endothelial repair and inhibition of vascular smooth muscle proliferation, playing a protective role in cardiovascular health. NPR2 undergoes dimerization and ligand-induced conformational changes to activate its guanylyl cyclase domain, and its activity is modulated by post-translational modifications such as phosphorylation. Research indicates that NPR2 plays an essential role in embryonic development and that its dysregulation may impact tissue regeneration and repair processes. Pharmacological activation of NPR2 has been explored for treating conditions like dwarfism and vascular dysfunction, emphasizing its potential as a therapeutic target.