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A major step toward understanding this relationship occurred when we determined that the AT4 receptor antagonist Norleual-AngIV (Nle-Tyr-Leu-(CH2-NH2)3-4-His-Pro-Phe) inhibited HGF binding to Met and HGF-dependent cell signaling, proliferation, invasion, and scattering [81]

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The production and secretion of chemokines responsible for the migration and accumulation of these inflammatory cells at the site of inflammation also appear to be stimulated by TNF- [15,16]
