Print Email Facebook Twitter Binding and degradation of tissue-type plasminogen activator by the human hepatoma cell line Hep G2 Title Binding and degradation of tissue-type plasminogen activator by the human hepatoma cell line Hep G2 Author Otter, M. van Berkel, T.J.C. Rijken, D.C. Gaubius Instituut TNO Publication year 1989 Abstract In this study, binding and degradation of tissue-type plasminogen activator (t-PA) by the human hepatoma cell line Hep G2 was investigated. Binding at 4°C was time-dependent and reached a maximum after ca. 2 hours. Scatchard analysis of saturation experiments showed about 170,000 high affinity binding sites for t-PA per cell with an apparent Kd of 90 nM. These binding sites were calcium-dependent. Part of the binding to the hepatoma cells was non-saturable, owing to a large amount of low affinity binding sites which are at least partially located on the extracellular matrix of the cells. Competition with mannose- and galactose-terminated glycoproteins had no effect on total binding of 125I-t-PA. Degradation products of 125I-t-PA were found in the supernatant after a short lag phase and then increased linearly for at least 5 hours at 37°C. Degradation could be inhibited by chloroquine, NH4Cl and NaN3. We conclude that the human hepatoma cell line Hep G2 has a specific binding mechanism for t-PA which is not mediated by known carbohydrate receptor systems. Binding is followed by cellular uptake and degradation in the lysosomes. Chemicals/CAS: tissue plasminogen activator, 105913-11-9; Calcium, 7440-70-2; Tissue Plasminogen Activator, EC 188.8.131.52 Subject Biologycatabolismcell culturecell lineliver cell carcinomapriority journalBinding, CompetitiveCalciumHumanLiverProtein BindingSupport, Non-U.S. Gov'tTissue Plasminogen ActivatorTumor Cells, Cultured To reference this document use: http://resolver.tudelft.nl/uuid:86da2369-0b93-4eac-af43-c2c9904fdcd7 TNO identifier 230795 ISSN 0340-6245 Source Thrombosis and Haemostasis, 62 (2), 667-672 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.