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    A dual, non-redundant, role for LIF as a regulator of development and STAT3-mediated cell death in mammary gland.

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    Authors
    Kritikou, Ekaterini A
    Sharkey, Andrew
    Abell, Kathrine
    Came, Paul J
    Anderson, Elizabeth
    Clarkson, Richard W E
    Watson, Christine J
    Affiliation
    Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK.
    Issue Date
    2003-08
    
    Metadata
    Show full item record
    Abstract
    STAT3 is the key mediator of apoptosis in mammary gland. We demonstrate here that LIF is the physiological activator of STAT3, because in involuting mammary glands of Lif(-/-) mice, pSTAT3 is absent and the STAT3 target, C/EBPdelta, is not upregulated. Similar to Stat3 knockouts, Lif(-/-) mammary glands exhibit delayed involution, reduced apoptosis and elevated levels of p53. Significantly, Lif(-/-) glands display precocious development during pregnancy, when pSTAT3 is not normally detected. We show that pERK1/2 is significantly reduced in Lif(-/-) glands at this time, suggesting that at this stage LIF mediates its effects through pERK1/2. Inhibition of LIF-mediated ERK1/2 phosphorylation potentiates the proapoptotic effects of STAT3. LIF therefore signals alternately through ERK1/2, then STAT3, to regulate mammary growth and apoptosis.
    Citation
    A dual, non-redundant, role for LIF as a regulator of development and STAT3-mediated cell death in mammary gland. 2003, 130 (15):3459-68 Development
    Journal
    Development
    URI
    http://hdl.handle.net/10541/82130
    DOI
    10.1242/dev.00578
    PubMed ID
    12810593
    Type
    Article
    Language
    en
    ISSN
    0950-1991
    ae974a485f413a2113503eed53cd6c53
    10.1242/dev.00578
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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