Probe-level estimation improves the detection of differential splicing in Affymetrix exon array studies 英文参考文献.docVIP
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Probe-level estimation improves the detection of differential splicing in Affymetrix exon array studies 英文参考文献
Open Access
Me d
2009LaajalaetVolul.metho10, Issue 7, Article R77
Probe-level estimation improves the detection of differential
splicing in Affymetrix exon array studies
Essi Laajala*, Tero Aittokallio*?, Riitta Lahesmaa* and Laura L Elo*?
Addresses: *Turku Centre for Biotechnology, University of Turku and ?bo Akademi University, Turku, FI-20521, Finland. ?Department of
Mathematics, University of Turku, Turku, FI-20014, Finland.
Correspondence: Laura L Elo. Email: laliel@utu.fi
Published: 16 July 2009
Received: 16 March 2009
Revised: 5 June 2009
Accepted: 16 July 2009
Genome Biology 2009, 10:R77 (doi:10.1186/gb-2009-10-7-r77)
The electronic version of this article is the complete one and can be
found online at /2009/10/7/R77
? 2009 Laajala et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which
permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
DetectingppA novedifferentiall statisticalsplicingprocedure is presented that uses probe-level information on Affymetrix exon arrays to detect differential splicing./
Abstract
The recent advent of exon microarrays has made it possible to reveal differences in alternative
splicing events on a global scale. We introduce a novel statistical procedure that takes full advantage
of the probe-level information on Affymetrix exon arrays when detecting differential splicing
between sample groups. In comparison to existing ranking methods, the procedure shows superior
reproducibility and accuracy in distinguishing true biological findings from background noise in high
agreement with experimental validations.
Background
eases [5,6]. In particular, a number of genetic point muta-
tions associated with human hereditary diseases have been
linked to disrupted splicing [6]. Hence, a comprehensive
understanding of
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