Year: 1999
Type: dissertation
Abstract: These authors contributed equally to the work.al., 1992), suggesting that bFGF-HSPG complexes serve as the biological active form of this growth factor.Cell surface heparin-like molecules are also involved in binding of VEGF to its high affinity receptor sites (Gitay-Goren et al., 1992).Released FGF can be sequestered from its site of action by binding to HS in the ECM (Vlodavsky et al., 1991;Bashkin et al., 1989) and saved for emergencies, such as wound repair and neovascularization (Vlodavsky et al., 1993).
Source: Työväentutkimus Vuosikirja
Author: Athina Lymboussaki
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Funder: Helsingin Yliopisto
OpenAlex ID: W2168206164