Figure 3: (1–3) Hypoxia induces PTP-1B and Src kinase. In this paradigm, ROS are shown as a mediator for this effect. Inflammatory pathways could also culminate to the activation of Src and PTP-1B. (4, 5) Src kinase phosphorylates and interferes with PTP-1B action. Use of PP2 (an Src kinase inhibitor) would ameliorate the effects of Src kinase and hence would inhibit PTP-1B production as shown in this study. Nitric oxide synthase might also interfere in this pathway. NO production was increased in cells overexpressing PTP-1B and treatment with PP2 significantly decreased its production. (6) Src kinase has a negative regulatory phosphorylation site (tyrosine-527). PTP-1B is found to dephosphorylate Src kinase at this residue. Tyr-527 occupies the carboxy-proximal area of Src and phosphorylation at this site has been shown to deactivate the enzyme. PTP-1B dephosphorylates and activates Src. (7) Under different circumstances, PTPs may dephosphorylate specific components of the Src kinase-associated complexes and lead to an actual disassembly of those and loss of their activity.