Abstract
We have previously reported the alternatively spliced transcripts of fibroblast growth factor receptor (FGFR) 3 derived by aberrant splicing in human cancers. Here, we describe a novel splice variant of FGFR2 (FGFR2DeltaIII) arising from skipping exons 7-10, resulting in the deletion of Ig-like-III domain in human chondrosarcoma cell. Sf9 cells expressing FGFR2DeltaIII were able to bind FGF1, FGF2, and FGF7, leading to loss of ligand-binding specificity. Together with our previous findings, the present studies suggest that mRNA splicing plays an important role in the regulation of FGFRs' function.
Copyright 2002 Elsevier Science Ireland Ltd.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Blotting, Western
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Chondrosarcoma / genetics*
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Chondrosarcoma / metabolism
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DNA Primers / chemistry
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Exons / genetics
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Fibroblast Growth Factor 1 / metabolism
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Fibroblast Growth Factor 2 / metabolism
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Fibroblast Growth Factor 7
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Fibroblast Growth Factors / metabolism
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Heparin / metabolism
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Humans
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Ligands
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Phosphotyrosine / metabolism
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Plasmids
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Protein Binding
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RNA Splicing / genetics*
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RNA, Messenger / metabolism
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Receptor Protein-Tyrosine Kinases / genetics*
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Receptor Protein-Tyrosine Kinases / metabolism
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Receptor, Fibroblast Growth Factor, Type 2
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Receptors, Fibroblast Growth Factor / genetics*
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Receptors, Fibroblast Growth Factor / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Sequence Deletion
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Tumor Cells, Cultured
Substances
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DNA Primers
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FGF7 protein, human
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Ligands
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RNA, Messenger
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Receptors, Fibroblast Growth Factor
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Fibroblast Growth Factor 2
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Fibroblast Growth Factor 1
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Fibroblast Growth Factor 7
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Phosphotyrosine
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Fibroblast Growth Factors
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Heparin
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FGFR2 protein, human
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Receptor Protein-Tyrosine Kinases
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Receptor, Fibroblast Growth Factor, Type 2