| Literature DB >> 11602259 |
B J Eggen1, G F Benus, S Folkertsma, L J Jonk, W Kruijer.
Abstract
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.Entities:
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Year: 2001 PMID: 11602259 DOI: 10.1016/s0014-5793(01)02928-3
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124