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  • Sir Peter MacCallum Department of Oncology
  • Sir Peter MacCallum Department of Oncology - Research Publications
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    Alternative Transcript Initiation and Splicing as a Response to DNA Damage

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    38
    Author
    Sprung, CN; Li, J; Hovan, D; Mckay, MJ; Forrester, HB
    Date
    2011-10-19
    Source Title
    PLoS One
    Publisher
    PUBLIC LIBRARY SCIENCE
    University of Melbourne Author/s
    Li, Jason
    Affiliation
    Sir Peter MacCallum Department of Oncology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Sprung, C. N., Li, J., Hovan, D., Mckay, M. J. & Forrester, H. B. (2011). Alternative Transcript Initiation and Splicing as a Response to DNA Damage. PLOS ONE, 6 (10), https://doi.org/10.1371/journal.pone.0025758.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259293
    DOI
    10.1371/journal.pone.0025758
    Abstract
    Humans are exposed to the DNA damaging agent, ionizing radiation (IR), from background radiation, medical treatments, occupational and accidental exposures. IR causes changes in transcription, but little is known about alternative transcription in response to IR on a genome-wide basis. These investigations examine the response to IR at the exon level in human cells, using exon arrays to comprehensively characterize radiation-induced transcriptional expression products. Previously uncharacterized alternative transcripts that preferentially occur following IR exposure have been discovered. A large number of genes showed alternative transcription initiation as a response to IR. Dose-response and time course kinetics have also been characterized. Interestingly, most genes showing alternative transcript induction maintained these isoforms over the dose range and times tested. Finally, clusters of co-ordinately up- and down-regulated radiation response genes were identified at specific chromosomal loci. These data provide the first genome-wide view of the transcriptional response to ionizing radiation at the exon level. This study provides novel insights into alternative transcripts as a mechanism for response to DNA damage and cell stress responses in general.

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