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. Author manuscript; available in PMC: 2019 Apr 17.
Published in final edited form as: J Am Chem Soc. 2018 Oct 15;140(42):13764–13774. doi: 10.1021/jacs.8b08014

Figure 2.

Figure 2.

ICP-MS measurements reveal that Cu supplementation via Gal-Cu(gtsm) is ASGPR-dependent. (A) ICP-MS studies comparing Cu levels upon 4 µM Cu-ionophore treatment (0.2% DMSO in serum-free DMEM) over a three-hour time course in HepG2 (ASGPR-expressing) cells. (B) ICP-MS studies upon 4 µM Cu-ionophore treatment (0.2% DMSO in serum-free DMEM) over a three-hour time course in HEK 293T (no ASGPR expression) cells. (C-D) HepG2 cells were treated with Gal-Cu(gtsm) (20 µM, C) or Cu(gtsm) (4 µM, D) over a one-hour period at either 4˚C or 37˚C. Data plotted relative to Cu/P ratio for each ionophore at 4˚C. (E) HepG2 cells were treated with or without D-galactose (1 M in serum-free DMEM) as a competitive ASGPR ligand fifteen minutes prior to treatment with vehicle, Cu(gtsm) (4 µM), or Gal-Cu(gtsm) (20 µM) over a one-hour period. Error bars = SEM (n = 6). Statistical analyses were performed using a one-way ANOVA with Bonferroni’s multiple comparisons test (A-B) or a two-tailed Student’s t test (C) where *P ≤ 0.05, ***P ≤ 0.001, and ****P ≤ 0.0001.