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    CD105 inhibits transforming growth factor-beta-Smad3 signalling.

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    Authors
    Guo, Baoqiang
    Slevin, Mark
    Li, Chenggang
    Parameshwar, Sudeep
    Liu, Donghui
    Kumar, Patricia
    Bernabeu, Carmelo
    Kumar, Shant
    Affiliation
    Laboratory Medicine Academic Group, Medical School, University of Manchester, Manchester, UK. Mqbssbg5@fs1.scg.man.ac.uk
    Issue Date
    2004
    
    Metadata
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    Abstract
    CD105 (endoglin) is an important component of the transforming growth factor-beta (TGF-beta) receptor complex and is highly expressed in endothelial cells in tissues undergoing angiogenesis such as healing wounds, infarcts and in a wide range of tumours. In an attempt to understand the molecular mechanism by which CD105 exerts its effects on angiogenesis by modulating TGF-beta1 signalling, in this preliminary communication, CD105 transfected rat myoblasts were utilized as an in vitro model. Overexpression of CD105 in these transfectants antagonised TGF-beta1-mediated inhibition of cell proliferation and reduced TGF-beta1-mediated p3TP-Lux (PAI-1 promoter) luciferase activity. It also reduced (CAGA)12-Luc luciferase activity in response to TGF-beta1. The CAGA sequence is specific for Smad3/4 binding, implying that CD105 is involved in inhibition of TGF-beta1/Smad3 signalling. Furthermore, CD105 overexpression reduced serine phosphorylation of Smad3 and inhibited subsequent nuclear translocation of Smad3. CD105 resulted in high phosphorylation of JNK1, which is able to activate c-Jun. c-Jun is known to inhibit Smad3 transcriptional activity on CAGA sites, suggesting that CD105 may also inhibit Smad3 signalling through JNK1.
    Citation
    CD105 inhibits transforming growth factor-beta-Smad3 signalling., 24 (3a):1337-45 Anticancer Res.
    Journal
    Anticancer Research
    URI
    http://hdl.handle.net/10541/77734
    PubMed ID
    15274293
    Type
    Article
    Language
    en
    ISSN
    0250-7005
    Collections
    All Christie Publications

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