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dc.contributor.authorPower, Karen A
dc.contributor.authorMcRedmond, James P
dc.contributor.authorde Stefani, Andreas
dc.contributor.authorGallagher, William M
dc.contributor.authorGaora, Peadar O
dc.date.accessioned2010-03-23T16:39:18Z
dc.date.available2010-03-23T16:39:18Z
dc.date.issued2009
dc.identifier.citationHigh-throughput proteomics detection of novel splice isoforms in human platelets. 2009, 4 (3):e5001 PLoS ONEen
dc.identifier.issn1932-6203
dc.identifier.pmid19308253
dc.identifier.doi10.1371/journal.pone.0005001
dc.identifier.urihttp://hdl.handle.net/10147/94732
dc.description.abstractAlternative splicing (AS) is an intrinsic regulatory mechanism of all metazoans. Recent findings suggest that 100% of multiexonic human genes give rise to splice isoforms. AS can be specific to tissue type, environment or developmentally regulated. Splice variants have also been implicated in various diseases including cancer. Detection of these variants will enhance our understanding of the complexity of the human genome and provide disease-specific and prognostic biomarkers. We adopted a proteomics approach to identify exon skip events - the most common form of AS. We constructed a database harboring the peptide sequences derived from all hypothetical exon skip junctions in the human genome. Searching tandem mass spectrometry (MS/MS) data against the database allows the detection of exon skip events, directly at the protein level. Here we describe the application of this approach to human platelets, including the mRNA-based verification of novel splice isoforms of ITGA2, NPEPPS and FH. This methodology is applicable to all new or existing MS/MS datasets.
dc.language.isoenen
dc.subject.meshAmino Acid Sequence
dc.subject.meshBlood Platelets
dc.subject.meshDatabases, Factual
dc.subject.meshExons
dc.subject.meshGenome, Human
dc.subject.meshHumans
dc.subject.meshMass Spectrometry
dc.subject.meshMetalloendopeptidases
dc.subject.meshPeptides
dc.subject.meshProtein Isoforms
dc.subject.meshProteomics
dc.subject.meshRNA, Messenger
dc.titleHigh-throughput proteomics detection of novel splice isoforms in human platelets.en
dc.contributor.departmentUCD Conway Institute and UCD School of Biomolecular & Biomedical Sciences, UCD Conway Institute, University College Dublin, Belfield, Dublin, Ireland.en
dc.identifier.journalPloS oneen
refterms.dateFOA2018-08-31T05:07:35Z
html.description.abstractAlternative splicing (AS) is an intrinsic regulatory mechanism of all metazoans. Recent findings suggest that 100% of multiexonic human genes give rise to splice isoforms. AS can be specific to tissue type, environment or developmentally regulated. Splice variants have also been implicated in various diseases including cancer. Detection of these variants will enhance our understanding of the complexity of the human genome and provide disease-specific and prognostic biomarkers. We adopted a proteomics approach to identify exon skip events - the most common form of AS. We constructed a database harboring the peptide sequences derived from all hypothetical exon skip junctions in the human genome. Searching tandem mass spectrometry (MS/MS) data against the database allows the detection of exon skip events, directly at the protein level. Here we describe the application of this approach to human platelets, including the mRNA-based verification of novel splice isoforms of ITGA2, NPEPPS and FH. This methodology is applicable to all new or existing MS/MS datasets.


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