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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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TAK1 activation of the mouse JunB promoter is mediated through a CCAAT box and NF-Y.

The JunB gene is activated by many stimuli including transforming growth factor beta (TGFbeta) family members and interleukin-6 ( IL-6). Here the effect of TGFbeta activated kinase 1 (TAK1), a mitogen activated protein kinase kinase kinase ( MAPKKK) implicated in TGFbeta, bone morphogenetic protein ( BMP) and interleukin-1 ( IL-1) signaling, on JunB promoter activity was investigated. Promoter analysis led to the identification of a CCAAT motif in the JunB gene, essential for activation by TAK1. Transfer of this CCAAT element to a heterologous minimal promoter conferred TAK1-responsiveness. The CCAAT-binding transcription factor, nuclear factor Y (NF-Y), activated the JunB promoter and a dominant negative NF-YA construct inhibited TAK1 activation of JunB. Our results demonstrate that JunB gene activation by TAK1 is mediated by the CCAAT-binding factor NF-Y.[1]

References

  1. TAK1 activation of the mouse JunB promoter is mediated through a CCAAT box and NF-Y. Eggen, B.J., Benus, G.F., Folkertsma, S., Jonk, L.J., Kruijer, W. FEBS Lett. (2001) [Pubmed]
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