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    Sensitisation of c-MYC-induced B-lymphoma cells to apoptosis by ATF2.

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    Authors
    Walczynski, J
    Lyons, Steve
    Jones, Nic
    Breitwieser, Wolfgang
    Affiliation
    Department of Cell Regulation, Paterson Institute for Cancer Research, University of Manchester, Manchester, UK.
    Issue Date
    2013-02-18
    
    Metadata
    Show full item record
    Abstract
    Transcription factors ATF2 (activating transcription factor 2) and ATF7 (activating transcription factor 7) are highly homologous members of the activator protein 1 (AP-1) family. Their activities are growth factor and stress stimulated and they strictly require phosphorylation by mitogen-activated protein (MAP) kinases for their transcriptional functions. In samples of human B-cell lymphomas as well as Eμ-Myc-driven mouse B-cell lymphomas, we find that ATF2 as well as MAP kinase c-Jun N-terminal kinase (JNK) are significantly up-regulated compared with normal human B-cell lines and mouse B cells, respectively. The B cell-specific deletion of ATF2 and ATF7 in mice results in significantly accelerated onset of Eμ-Myc-induced lymphoma. In addition, loss of ATF2/7 desensitises Eμ-Myc lymphoma cells to spontaneous as well as stress-induced apoptosis. Our results therefore suggest that c-MYC induces stress-mediated activation of ATF2 and ATF7 and that these transcription factors regulate apoptosis in response to oncogenic transformation of B cells.Oncogene advance online publication, 18 February 2013; doi:10.1038/onc.2013.28.
    Citation
    Sensitisation of c-MYC-induced B-lymphoma cells to apoptosis by ATF2. 2013: Oncogene
    Journal
    Oncogene
    URI
    http://hdl.handle.net/10541/273000
    DOI
    10.1038/onc.2013.28
    PubMed ID
    23416976
    Type
    Article
    Language
    en
    ISSN
    1476-5594
    ae974a485f413a2113503eed53cd6c53
    10.1038/onc.2013.28
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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