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Results clearly present the chemical potentiation of LASSS on physiological functions of HGF, as revealed by enhanced receptor-binding affinity and nitration-dysfunction resistance through interaction/reaction with LASSS under physiological conditions
Finally, GSH depletion was designated as necessary to induce the redox unbalance characteristic of the induction phase of the mitochondrial pathway but not sufficient per se to assure the execution phase of apoptosis
Supports immune function
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