Figure 10: Principle of the NP-based cell chip. Upon interaction of the negatively charged reporter enzyme, GPI-β-galactosidase, with cationic hydrophobic gold-NPs, the positively charged complexes consisting of NPs and GPI-β- galactosidase come into contact with the outer leaflet of the plasma membrane bilayer and are subsequently translocated to the surface phospholipid monolayer of the cytoplasmic lipid droplets. Upon arrival at the cytoplasm with accumulated correctly folded or aggregated misfolded polypeptides, the NPs either remain bound or are relieved from binding to the GPI-β-galactosidase. The resulting inhibition or activation, respectively, of GPI-β-galactosidase is monitored as light generation and indicative for the amount of ectopically expressed passenger protein drug in the recombinant host cells that differs in structure from the authentic product.