SU11274, another ATP-competitive c-MET selective inhibitor, blocked the constitutive phosphorylation of c-MET and downstream kinases and induced G2/M cell cycle arrest and significantly suppressed cell growth in a dose-dependent manner [42]
This reveals that glutathione binds in the G site in a very similar fashion as the glutathione portion of substrate analogues in other structures and also that glutathione binding alone is sufficient to stabilize the C-terminal helix of the protein
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