Literature DB >> 18508431

Diagnostics of pathogenic splicing mutations: does bioinformatics cover all bases?

Linda Hartmann1, Stephan Theiss, Dieter Niederacher, Heiner Schaal.   

Abstract

Pathogenic splicing alterations caused by point mutations in both splice sites and auxiliary cis-regulatory elements are increasingly recognized as an important mechanism through which gene mutations cause human disease. Unfortunately, in routine genetic diagnostic settings, splicing mutations may escape identification, due to the lack of RNA samples. Since most patients are genotyped only, any computational prediction of mutation effects on splicing can be beneficial for the human geneticist. Here, we review common techniques to identify human point mutations and delineate the molecular basis for splice site recognition. Moreover, this article provides basic insights into web-tools predicting splice sites and cis-regulatory elements and discusses their benefits for judgment of clinically identified sequence variants of disease-specific genes.

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Year:  2008        PMID: 18508431     DOI: 10.2741/2924

Source DB:  PubMed          Journal:  Front Biosci        ISSN: 1093-4715


  25 in total

1.  Excessive RNA splicing and inhibition of HIV-1 replication induced by modified U1 small nuclear RNAs.

Authors:  Dibyakanti Mandal; Zehua Feng; C Martin Stoltzfus
Journal:  J Virol       Date:  2010-10-06       Impact factor: 5.103

Review 2.  Adult-onset presentations of genetic immunodeficiencies: genes can throw slow curves.

Authors:  Katharine S Nelson; David B Lewis
Journal:  Curr Opin Infect Dis       Date:  2010-08       Impact factor: 4.915

3.  Widespread recognition of 5' splice sites by noncanonical base-pairing to U1 snRNA involving bulged nucleotides.

Authors:  Xavier Roca; Martin Akerman; Hans Gaus; Andrés Berdeja; C Frank Bennett; Adrian R Krainer
Journal:  Genes Dev       Date:  2012-05-15       Impact factor: 11.361

Review 4.  Missed threads. The impact of pre-mRNA splicing defects on clinical practice.

Authors:  Diana Baralle; Anneke Lucassen; Emanuele Buratti
Journal:  EMBO Rep       Date:  2009-08       Impact factor: 8.807

5.  Genomic HEXploring allows landscaping of novel potential splicing regulatory elements.

Authors:  Steffen Erkelenz; Stephan Theiss; Marianne Otte; Marek Widera; Jan Otto Peter; Heiner Schaal
Journal:  Nucleic Acids Res       Date:  2014-08-21       Impact factor: 16.971

6.  Splicing defects caused by exonic mutations in PKD1 as a new mechanism of pathogenesis in autosomal dominant polycystic kidney disease.

Authors:  Felix Claverie-Martin; Francisco J Gonzalez-Paredes; Elena Ramos-Trujillo
Journal:  RNA Biol       Date:  2015       Impact factor: 4.652

7.  Assessment of the F9 genotype-specific FIX inhibitor risks and characterisation of 10 novel severe F9 defects in the first molecular series of Argentinian patients with haemophilia B.

Authors:  Claudia Pamela Radic; Liliana Carmen Rossetti; Miguel Martín Abelleyro; Miguel Candela; Raúl Pérez Bianco; Miguel de Tezanos Pinto; Irene Beatriz Larripa; Anne Goodeve; Carlos Daniel De Brasi
Journal:  Thromb Haemost       Date:  2012-10-23       Impact factor: 5.249

8.  Genomic features defining exonic variants that modulate splicing.

Authors:  Adam Woolfe; James C Mullikin; Laura Elnitski
Journal:  Genome Biol       Date:  2010-02-16       Impact factor: 13.583

9.  Recognition of atypical 5' splice sites by shifted base-pairing to U1 snRNA.

Authors:  Xavier Roca; Adrian R Krainer
Journal:  Nat Struct Mol Biol       Date:  2009-01-25       Impact factor: 15.369

10.  Functional properties and evolutionary splicing constraints on a composite exonic regulatory element of splicing in CFTR exon 12.

Authors:  Ariful Haque; Emanuele Buratti; Francisco E Baralle
Journal:  Nucleic Acids Res       Date:  2009-11-12       Impact factor: 16.971

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