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This initial phosphorylation cascade leads to autophosphorylation of the carboxy-terminal bidentate substrate-binding site (Tyr1349 and Tyr1356) of the c-Met and these residues have been shown as docking sites for downstream signaling molecules [52]
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This combination has been utilized in preclinical studies examining growth factor receptor signaling, angiogenesis pathway activity, actin polymerization dynamics, gut epithelial cell function, and nitric oxide pathway interactions independent of the broader biological effects associated with endogenous BPC and Thymosin Beta-4 activity
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