Traceable biochemistry claims

Molecular mechanism of AFB1 genotoxicity

Evidence supports metabolism-dependent AFBO formation and persistent FAPy lesions as important drivers, but mutation risk also depends on repair, replication context, lesion persistence, and clonal selection rather than total adduct count alone.

Test hepatocyte lesions, repair, and mutations
Compare FAPy persistence with mutation spectra

Dopamine biosynthesis across kingdoms

The supplied evidence distinguishes a plant tyramine pathway involving TyDC and PPO from mammalian TH-centered control, while pathway flux, developmental timing, and tissue context remain important limits on direct cross-kingdom comparisons.

Measure plant TyDC and PPO pathway flux
Track TH-dependent flux during development

PFK-1 allosteric control of glycolysis

Biochemical and structural evidence supports ATP as a negative regulator that signals energy abundance, while fructose-2,6-bisphosphate activates PFK-1 and can counter ATP inhibition; cellular effects depend on metabolite concentrations and hormonal state.

Test ATP and F-2,6-BP interaction with flux