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The primary mode of action for these bacteriocins involves either pore formation in the target cell membrane or inhibition of cell wall synthesis, ultimately resulting in bacterial cell death (196, 197)

The counter GSSSG treatment did not increase activation activity of 1 ng/ml HGF ( left orange-bar ), consistent with the earlier observation that GSSSG did not effectively modulate the HGF-c-met interaction (Figure 1e right column, orange bars 4 and 5 ), and hence served as a control trisulfide

This regulation is absent in c-Met-deficient primary mouse hepatocytes, leading to the overproduction of ROS, increased oxidative stress, and heightened sensitivity to apoptosis-promoting agents