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TAK1 activation of the mouse JunB promoter is mediated through a CCAAT box and NF‐Y
Author(s) -
Eggen B.J.L.,
Benus G.F.J.D.,
Folkertsma S.,
Jonk L.J.,
Kruijer W.
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02928-3
Subject(s) - junb , fosb , microbiology and biotechnology , caat box , transcription factor , map kinase kinase kinase , biology , kinase , promoter , protein kinase a , gene expression , gene , genetics
The JunB gene is activated by many stimuli including transforming growth factor β (TGFβ) family members and interleukin‐6 (IL‐6). Here the effect of TGFβ activated kinase 1 (TAK1), a mitogen activated protein kinase kinase kinase (MAPKKK) implicated in TGFβ, 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.