Abstract
Alu repetitive elements can be inserted into mature messenger RNAs via a splicing-mediated process termed exonization. To understand the molecular basis and the regulation of the process of turning intronic Alus into new exons, we compiled and analyzed a data set of human exonized Alus. We revealed a mechanism that governs 3' splice-site selection in these exons during alternative splicing. On the basis of these findings, we identified mutations that activated the exonization of a silent intronic Alu.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Deaminase / genetics
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Alternative Splicing*
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Alu Elements / genetics*
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Cell Line
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Cloning, Molecular
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DNA, Antisense
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Dinucleoside Phosphates / genetics
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Exons*
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Genome, Human
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Glucosyltransferases / genetics
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Humans
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Introns
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Mutagenesis, Site-Directed
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Point Mutation
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Polymerase Chain Reaction
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RNA Splicing Factors
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RNA-Binding Proteins
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Ribonucleoproteins, Small Nuclear / genetics
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Ribonucleoproteins, Small Nuclear / physiology
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Spliceosomes / metabolism
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Transfection
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Tumor Cells, Cultured
Substances
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DNA, Antisense
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Dinucleoside Phosphates
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RNA Splicing Factors
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RNA-Binding Proteins
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Ribonucleoproteins, Small Nuclear
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SLU7 protein, human
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adenylyl-(3'-5')-guanosine
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Glucosyltransferases
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ADARB1 protein, human
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Adenosine Deaminase