Catabolism of human low density lipoproteins by human hepatoma cell line HepG2.
作者： Nassrin Dashti , Gertrud Wolfbauer , Eugen Koren , Barbara Knowles , Peter Alaupovic
DOI: 10.1016/0005-2760(84)90003-1
关键词:
摘要: The mechanism of hepatic catabolism human low density lipoproteins (LDL) by human-derived hepatoma cell line HepG2 was studied. binding 125I-labeled LDL to cells at 4 degrees C time dependent and inhibited excess unlabeled LDL. specific predominant concentrations (less than 50 micrograms protein/ml), whereas the nonsaturable prevailed higher substrate. cellular uptake degradation were curvilinear functions substrate concentration. Preincubation with caused a 56% inhibition in Reductive methylation abolished its ability compete for degradation. Chloroquine (50 microM) colchicine (1 64% 30%, respectively. suppressed de novo synthesis cholesterol enhanced esterification; this stimulation chloroquine. When tested similar content apolipoprotein B, very (VLDL), high (HDL) same degree, indicating that normal are most probably recognized receptor via B. current study thus demonstrates proceeds part through receptor-mediated mechanism.
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