Characterization of the murine BEK fibroblast growth factor (FGF) receptor: activation by three members of the FGF family and requirement for heparin.
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 articleSubject
Amino Acid SequenceAnimals
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
Permalink
https://hdl.handle.net/10161/8400Collections
More Info
Show full item recordScholars@Duke
Sally A. Kornbluth
Jo Rae Wright University Distinguished Professor Emerita
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

Articles written by Duke faculty are made available through the campus open access policy. For more information see: Duke Open Access Policy
Rights for Collection: Scholarly Articles
Works are deposited here by their authors, and represent their research and opinions, not that of Duke University. Some materials and descriptions may include offensive content. More info
Related items
Showing items related by title, author, creator, and subject.
-
Fibroblast growth factor 23 is not associated with and does not induce arterial calcification.
Scialla, Julia J; Lau, Wei Ling; Reilly, Muredach P; Isakova, Tamara; Yang, Hsueh-Ying; Crouthamel, Matthew H; Chavkin, Nicholas W; ... (23 authors) (Kidney international, 2013-06)Elevated fibroblast growth factor 23 (FGF23) is associated with cardiovascular disease in patients with chronic kidney disease. As a potential mediating mechanism, FGF23 induces left ventricular hypertrophy; however, its ... -
Fibroblast growth factor23 is associated with axonal integrity and neural network architecture in the human frontal lobes.
Marebwa, Barbara K; Adams, Robert J; Magwood, Gayenell S; Kindy, Mark; Wilmskoetter, Janina; Wolf, Myles; Bonilha, Leonardo (PloS one, 2018-01)Elevated levels of FGF23 in individuals with chronic kidney disease (CKD) are associated with adverse health outcomes, such as increased mortality, large vessel disease, and reduced white matter volume, cardiovascular and ... -
Fibroblast growth factor-23-mediated inhibition of renal phosphate transport in mice requires sodium-hydrogen exchanger regulatory factor-1 (NHERF-1) and synergizes with parathyroid hormone.
Weinman, Edward J; Steplock, Deborah; Shenolikar, Shirish; Biswas, Rajatsubhra (The Journal of biological chemistry, 2011-10)Fibroblast growth factor-23 (FGF-23) inhibits sodium-dependent phosphate transport in brush border membrane vesicles derived from hormone-treated kidney slices of the mouse and in mouse proximal tubule cells by processes ...