(PDF) An Intronic Splicing Silencer Causes Skipping of the

An Intronic Splicing Silencer Causes Skipping of the IIIb Exon of Fibroblast Growth Factor Receptor 2 Through Involvement of Polypyrimidine Tract Binding Protein

Molecular and Cellular Biology - United States

doi 10.1128/mcb.20.19.7388-7400.2000

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Date

October 1, 2000

Authors

R. P. Carstens

E. J. Wagner

M. A. Garcia-Blanco

Publisher

American Society for Microbiology

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An Intronic Splicing Silencer Causes Skipping of the IIIb Exon of Fibroblast Growth Factor Receptor 2 Through Involvement of Polypyrimidine Tract Binding Protein

Molecular and Cellular Biology - United States

doi 10.1128/mcb.20.19.7388-7400.2000

Full Text

Abstract

Categories

Date

Authors

Publisher

Related search

A New Regulatory Protein, KSRP, Mediates Exon Inclusion Through an Intronic Splicing Enhancer.

Sequence Requirements for Regulated RNA Splicing of the Human Fibroblast Growth Factor Receptor-1 Α Exon

Exon Skipping Through the Creation of a Putative Exonic Splicing Silencer as a Consequence of the Cystic Fibrosis Mutation R553X

The Polypyrimidine Tract Binding Protein Binds Upstream of Neural Cell-Specific C-SRC Exon N1 to Repress the Splicing of the Intron Downstream.

The Polypyrimidine Tract Binding Protein (PTB) Represses Splicing of Exon 6B From the -Tropomyosin Pre-mRNA by Directly Interfering With the Binding of the U2AF65 Subunit

Distinct Factor Requirements for Exonic Splicing Enhancer Function and Binding of U2AF to the Polypyrimidine Tract

Multiple Splicing Defects in an Intronic False Exon

Oligomerization Reduces Heparin Affinity but Enhances Receptor Binding of Fibroblast Growth Factor 2

Differential Splicing in the Extracellular Region of Fibroblast Growth Factor Receptor 1 Generates Receptor Variants With Different Ligand-Binding Specificities.