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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Curr Opin Immunol. 2015 Nov 14;38:24–29. doi: 10.1016/j.coi.2015.10.006

Figure 2. Localized signals open junctions for transmigration.

Figure 2

The diagram depicts two processes critical for TEM: targeted recycling of the LBRC and disruption of VE-cadherin at the site of TEM. PECAM-PECAM interactions between leukocyte and endothelial cell trigger signals that activate ↑[Ca+2]i through TRPC6 to recruit the LBRC to the site of TEM. VLA-4 on leukocytes interacts with VCAM-1 on EC to activate Rac1, which activates NADPH oxidase (NOX) to generate reactive oxygen species (ROS) that activate the kinase Pyk2. This phosphorylates a putative substrate for vascular endothelial receptor protein tyrosine phosphatase (VE-PTP), which reduces the affinity of VE-PTP for VE-cadherin, favoring phosphorylation (circled P) of VE-cadherin and its removal from the adherens junction.