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Characterization of the murine BEK fibroblast growth factor (FGF) receptor: activation by three members of the FGF family and requirement for heparin.

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Date
1992-04-15
Authors
Mansukhani, A
Dell'Era, P
Moscatelli, D
Kornbluth, S
Hanafusa, H
Basilico, C
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Abstract
The bek gene encodes a member of the high-affinity fibroblast growth factor receptor family. The BEK/FGFR-2 receptor is a membrane-spanning tyrosine kinase with the typical features of FGF receptors. We have cloned a murine bek cDNA and expressed it in receptor-negative Chinese hamster ovary cells and in 32D myeloid cells. The BEK receptor expressed in Chinese hamster ovary cells binds acidic FGF, basic FGF, and Kaposi FGF equally well but does not bind keratinocyte growth factor or FGF-5 appreciably. Upon treatment with basic FGF or Kaposi FGF, the BEK receptor is phosphorylated and a mitogenic response is achieved. Heparan sulfate proteoglycans have been shown to play an obligate role in basic FGF binding to the high-affinity FLG receptor. Unlike the BEK-expressing Chinese hamster ovary cells, 32D cells expressing the BEK receptor require the addition of exogenous heparin in order to grow in the presence of basic FGF or Kaposi FGF. We show that the addition of heparin greatly enhances the binding of radio-labeled basic FGF to the receptor. Thus the BEK receptor, like FLG, also requires an interaction with heparan sulfate proteoglycans to facilitate binding to its ligands.
Type
Journal article
Subject
Amino Acid Sequence
Animals
Binding, Competitive
CHO Cells
Cell Division
Cell Line
Cloning, Molecular
Cricetinae
DNA
Fibroblast Growth Factor 1
Fibroblast Growth Factor 2
Fibroblast Growth Factors
Gene Library
Heparin
Kinetics
Male
Molecular Sequence Data
Protein-Tyrosine Kinases
Receptors, Cell Surface
Receptors, Fibroblast Growth Factor
Transfection
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https://hdl.handle.net/10161/8400
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Scholars@Duke

Kornbluth

Sally A. Kornbluth

Jo Rae Wright University Distinguished Professor
Our lab studies the regulation of complex cellular processes, including cell cycle progression and programmed cell death (apoptosis). These tightly orchestrated processes are critical for appropriate cell proliferation and cell death, and when they go awry can result in cancer and degenerative disorders. Within these larger fields, we have focused on understanding the cellular mechanisms that prevent the onset of mitosis prior to the completion of DNA replication, the process
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