Receptor-type tyrosine-protein phosphatase beta (PTPRB)

Receptor-type tyrosine-protein phosphatase beta (PTPRB), also known as vascular endothelial protein tyrosine phosphatase (VE-PTP), is a transmembrane enzyme primarily expressed in vascular endothelial cells [1, 2]. It plays a crucial role in maintaining vascular stability by regulating the phosphorylation state of key endothelial proteins, most notably the Tie2 receptor tyrosine kinase and VE-cadherin [4]. Under physiological conditions, PTPRB dephosphorylates Tie2, acting as a molecular brake on the signaling pathways that promote vessel maturation and survival. In diseases such as diabetic retinopathy and macular edema, overactivity or presence of PTPRB contributes to vascular leakage and pathological angiogenesis [3]. Therapeutic strategies targeting PTPRB involve small molecule inhibitors like razuprotafib (AKB-9778), which block its phosphatase activity to restore Tie2 signaling and stabilize the blood-retinal barrier [5]. Additionally, PTPRB is involved in the regulation of inflammatory cell recruitment and has been investigated for its role in tumor angiogenesis, making it a significant target for both ocular and systemic vascular disorders [1, 4].

Other names

VE-PTPVascular endothelial protein tyrosine phosphataseHPTPBPTPBR-PTP-beta

Inhibition of PTPRB (VE-PTP) catalytic activity prevents the dephosphorylation of the Tie2 receptor tyrosine kinase, leading to Tie2 activation and subsequent stabilization of the vascular endothelium.