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Moreover, our cell-based activity assays showed that the HGF with mutations that disrupt either K1–SEMA or SPH–SEMA interaction no longer activated c-MET, but the HGF with mutations that disrupt either N–SEMA, K2–SEMA, or K3–SEMA interaction still exhibited partial activity, suggesting that the K1–SEMA and SPH–SEMA interfaces are more critical for HGF-induced c-MET activation than any other interfaces