Activation of junB by PKC and PKA signal transduction through a novel cis-acting element

• Published in: Nucleic acids research 1991-02, Vol.19 (4), p.775-781
• Main Authors: DE GROOT, R. P, AUWERX, J, KARPERIEN, M, STAELS, B, KRUIJER, W
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Biological and medical sciences; Blood; Blotting, Northern; Cross-Linking Reagents; DNA-Binding Proteins - genetics; Fundamental and applied biological sciences. Psychology; Mice; Molecular and cellular biology; Molecular genetics; Molecular Sequence Data; Plasmids; Promoter Regions, Genetic; Protein Kinase C - metabolism; Protein Kinases - metabolism; Proto-Oncogene Proteins c-jun; RNA - analysis; Signal Transduction; Transcription Factors - genetics; Transcription. Transcription factor. Splicing. Rna processing; Transfection; Tumor Cells, Cultured
• ISSN: 0305-1048; 1362-4962
• DOI: 10.1093/nar/19.4.775

The product of the junB gene, a gene homologous to the proto-oncogene c-jun, is a component of transcription factor AP-1. JunB expression is modulated by a wide variety of extracellular stimuli, such as serum, growth factors, phorbol esters (TPA) and activators of protein kinase A (PKA). In order to study the molecular basis of this complex regulation, we have cloned the mouse junB gene from a genomic testis library, and characterized the junB promoter. Here we show that the junB promoter is activated by serum, TPA, and activated PKA. Sequences located between -91 and -44 are necessary for induction. These sequences contain a CAAT box, a G-C rich region and a previously undescribed inverted repeat (IR). The IR element can mediate induction by TPA and PKA when coupled to a heterologous promoter, and specifically binds a protein of 110 kD.