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In addition to different signal strength, the distinct conformation of c-MET triggered by different types of ligand may allow it to preferentially activate different downstream signaling pathways through engaging distinct sets of downstream effectors, which is reminiscent of the biased agonism paradigm established for other RTKs, such as EGFR 35

Journal of Translational Medicine, 22(1), Article 86

TB-500 acts as a potent endothelial cell chemoattractant, stimulating 4-6-fold increases in HUVEC migration[4]