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Biochem Biophys Res Commun. 1993 Jul 15;194(1):512-8.

Exon skipping causes alteration of the COOH-terminus and deletion of the phospholipase C gamma 1 interaction site in the FGF receptor 2 kinase in normal prostate epithelial cells.

Author information

1
W. Alton Jones Cell Science Center, Inc., Lake Placid, NY 12946.

Abstract

Polymerase chain reaction analysis revealed an mRNA in rat prostate that results from alternate splicing of exon 16 in the heparin-binding fibroblast growth factor receptor kinase type 2 gene (FGFR2). The absence of exon 16 and the shift in reading frame at the exon 15-17 junction predicts an expression product (FGFR2-2) with a unique COOH-terminus that does not exhibit the major autophosphorylation site (tyrosine 789) required for interaction of phospholipase C gamma 1 with the full-length FGFR2-1 isoform. Nuclease protection analysis revealed that the FGFR-2 splice variant is expressed in quantities equal to or greater than the FGFR2-1 isoform in normal prostate tissue. When combined with the same FGFR2 extracellular domain, co-expression of the two COOH-terminal variants may mediate effect of the same FGF ligand on different signal transduction pathways.

PMID:
8333865
DOI:
10.1006/bbrc.1993.1849
[Indexed for MEDLINE]

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