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    Feedback regulation of p38 activity via ATF2 is essential for survival of embryonic liver cells.

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    Authors
    Breitwieser, Wolfgang
    Lyons, Steve
    Flenniken, Ann Marie
    Ashton, Garry
    Bruder, Gail
    Willington, Mark
    Lacaud, Georges
    Kouskoff, Valerie
    Jones, Nic
    Affiliation
    Cell Regulation Department, Paterson Institute for Cancer Research, University of Manchester, Manchester M20 4BX, United Kingdom.
    Issue Date
    2007-08-15
    
    Metadata
    Show full item record
    Abstract
    The ATF2 transcription factor is phosphorylated by the stress-activated mitogen-activated protein kinases (MAPKs) JNK and p38. We show that this phosphorylation is essential for ATF2 function in vivo, since a mouse carrying mutations in the critical phosphorylation sites has a strong phenotype identical to that seen upon deletion of the DNA-binding domain. In addition, combining this mutant with a knockout of the ATF2 homolog, ATF7, results in embryonic lethality with severe abnormalities in the developing liver and heart. The mutant fetal liver is characterized by high levels of apoptosis in developing hepatocytes and haematopoietic cells. Furthermore, we observe a significant increase in active p38 due to loss of a negative feedback loop involving the ATF2-dependent transcriptional activation of MAPK phosphatases. In embryonic liver cells, this increase drives apoptosis, since it can be suppressed by chemical inhibition of p38. Our findings demonstrate the importance of finely regulating the activities of MAPKs during development.
    Citation
    Feedback regulation of p38 activity via ATF2 is essential for survival of embryonic liver cells. 2007, 21 (16):2069-82 Genes Dev.
    Journal
    Genes & Development
    URI
    http://hdl.handle.net/10541/70357
    DOI
    10.1101/gad.430207
    PubMed ID
    17699753
    Type
    Article
    Language
    en
    ISSN
    0890-9369
    ae974a485f413a2113503eed53cd6c53
    10.1101/gad.430207
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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