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- W2003167913 abstract "Receptor-mediated endocytosis in suspended hepatocytes was studied in conjunction with ATP levels of the cells, which were decreased by the use of metabolic inhibitors. The receptor system studied was the asialo-glycoprotein receptor, and multiple aspects of the endocytic pathway were examined: binding of ligand, internalization, intracellular transport and proteolysis. (1) Moderate concentrations of the inhibitors (e.g. 30 μM rotenone or 200 μM iodoacetamide) produced only a transient decline in the ATP levels of the vells. Two to four times higher concentrations reduced the ATP levels to about 110 of control cells. (2) At low levels of ATP (less than 30% of controls) the uptake ceased completely after 10–20 min. Moderate reductions brought about by retenone reduced the uptake roughly in proportion to the ATP levels; iodoacetamide and sodium fluoride had little influence on the energy production by the cells, but the rate of asialo-glycoprotein uptake was reduced to a small fraction of controls. (3) The effect of rotenone on the rate of uptake was mainly due to a lower rate of internalization of occupied receptors; the half-time for internalization of surface-bound ligand was increased from 2.9 to 6.2 min in the presence of 42 μM rotenone. The binding capacity of the cell surface was also somewhat lower. (4) There was no degradation of the asialo-glycoproteins which were taken up by cells treated with high concentrations of rotenone or iodoacetamide. This was shown to be due to a low rate of transport of the endocytosed protein into those endosomes (at density 1.15 g/ml in a sucrose gradient) which were delivering their contents to the lysosomes; coincidentally, there was an accumulation of ligand in light endosomes (density 1.11 g/ml), in which the ligand appears immediately after endocytosis." @default.
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- W2003167913 date "1985-05-01" @default.
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- W2003167913 title "The influence of cellular ATP levels on receptor-mediated endocytosis and degradation of asialo-glycoproteins in suspended hepatocytes" @default.
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- W2003167913 doi "https://doi.org/10.1016/0006-2952(85)90628-8" @default.
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