High impact information on Ptprb

• VE-PTP, a receptor-type phosphotyrosine phosphatase, associates with the tyrosine kinase receptor Tie-2 and VE-cadherin and enhances the adhesive function of the latter [1].
• Vascular endothelial cell-specific phosphotyrosine phosphatase (VE-PTP) activity is required for blood vessel development [1].
• Here, VE-PTP was found to be restricted to endothelial cells, with a preference for arterial endothelium [1].
• Mutant mice expressing a truncated, secreted form of VE-PTP lacking the cytoplasmic and transmembrane domains and the most membrane-proximal extracellular fibronectin type III repeat, showed severe vascular malformations causing lethality at 10 days of gestation [1].
• In addition, VE-PTP dephosphorylates Tie-2 but not VEGFR-2 [2].

Biological context of Ptprb

• Based on its potential role as a regulator of blood vessel morphogenesis and maintainance, VE-PTP is a candidate gene for inherited vascular malformations similar to the Tie-2 gene [2].

Anatomical context of Ptprb

• Thus, the activity of VE-PTP is not required for the initial formation of blood vessels, yet it is essential for their maintenance and remodeling [1].

References