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. 2010 Jun 11;86(6):588–610. doi: 10.2183/pjab.86.588

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© 2010 The Japan Academy

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — A hypothetical model for injury-specific HGF/c-Met intracellular signaling. (A) In non-injurious (i.e., normal) organ tissues, a serine residue site at position 985 (Ser-985) in the juxtamembrane of c-Met is constitutively phosphorylated and functions as a negative regulator to inhibit HGF-Met signaling (i.e., switch OFF). (B) Once organ tissues undergo injuries, Ser-985 site is “de-”phosphorylated, probably via recruitment of intracellular PP2A. As a result, c-Met tyrosine sites are phospholylated, and then pleiotropic activities are delivered (i.e., switch ON).