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These new findings encourage a novel working hypothesis for further research, that a chemical-modification mechanism enables transformation of HGF through interaction or reaction with LASSS under physiological conditions, resulting in the retention of HGFs biological activity after exposure to peroxynitrite, at least until an enhanced form of HGF undergoes metabolic turnover in vivo

Conclusion: PFIC1-specific hiHeps can recapitulate the dysfunctional activity of FIC1 and support the hypothesis that dysregulated FXR contributes to the PFIC1 phenotype

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