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The binding of C-Met to HGF initiates the receptors innate kinase activity, followed by the formation of a multisubstrate docking site for the intracellular junction protein, which recruits signaling molecules due to homologous dimerization and autophosphorylation at Tyr1234 and Tyr1235 and subsequent phosphorylation at Tyr1349 and Tyr1356 at the c-terminal tail (Birchmeier et al., 2003

By enabling endothelial cell migration and tube formation, the actin-binding site drives pro-angiogenic activity a key step in granulation tissue and repair

Some report improvement in pain or mobility within a few weeks

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