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

• Published in: FEBS letters 2001-10, Vol.506 (3), p.267-271
• Main Authors: Eggen, B.J.L., Benus, G.F.J.D., Folkertsma, S., Jonk, L.J., Kruijer, W.
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; CCAAT motif; CCAAT-Binding Factor - metabolism; Cell Line; DNA; DNA Primers; EMSA, electrophoretic mobility shift assay; Gene Expression Regulation - genetics; Genes, Reporter; Humans; Interleukin-1 - physiology; JunB; Luciferases - genetics; MAP Kinase Kinase Kinases - metabolism; MAPK, mitogen activated protein kinase; Mice; NF-Y, nuclear factor Y; nt, nucleotides; Nuclear factor Y; Promoter; Promoter Regions, Genetic; Proto-Oncogene Proteins c-jun - genetics; Reverse Transcriptase Polymerase Chain Reaction; TAK1, transforming growth factor β activated kinase 1; TGFβ, transforming growth factor β; Transcriptional Activation; Transforming Growth Factor beta - physiology; Transforming growth factor β activated kinase 1
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(01)02928-3

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.