Fig. 1. The concept of MONOTAB based on lysosome-targeting endocytosis of NPs.

a Targeted degradation of extracellular proteins or vesicles mediated by MONOTABs. b Cellular uptake of rhodamine B-labeled NPs (^RBNPs) after co-incubation with B16F10 cells for 2 or 4 h (n = 3 biologically independent experiments, each counting 10,000 cells). c Live-cell imaging of different cell lines treated with ^RBNPs (100 μg mL⁻¹) for 4 h. Scale bar, 10 μm. The images are representative of n = 3 biological replicates. d Effects of endocytic inhibitors on cellular uptake of ^RBNPs in different cell lines in terms of the RB intensity measured by flow cytometry (n = 3 biologically independent experiments). e and f Cellular uptake of ^RBNPs (50 μg mL⁻¹) after co-incubation with Igf2r- or Tfrc-KO B16F10 cells, or Itgav-, Ackr3-, Ldlr-, Gba1-, Scarb1- or Vti1a-silencing B16F10 cells for 2 h (n = 3 biologically independent experiments, each counting 10,000 cells). g Cellular uptake of ^RBNPs (50 μg mL⁻¹) after co-incubation with B16F10 cells for 2 h. Cells were pre-treated with trypsin within 3 h (n = 3 biologically independent experiments, each counting 10,000 cells). Data are presented as mean ± SD where relevant. p values were determined by one-way analysis of variance (ANOVA) with Dunnett’s post hoc test. ns no significance; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Source data are provided as a Source Data file.