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Its unique peptide-metal structure provides researchers with a valuable model for investigating metal-dependent biological processes and the integration of signaling pathways within complex laboratory systems

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Moreover, our cell-based activity assays showed that the HGF with mutations that disrupt either K1SEMA or SPHSEMA interaction no longer activated c-MET, but the HGF with mutations that disrupt either NSEMA, K2SEMA, or K3SEMA interaction still exhibited partial activity, suggesting that the K1SEMA and SPHSEMA interfaces are more critical for HGF-induced c-MET activation than any other interfaces