1. ¹Department of Veterinary Biosciences and Center for Retrovirus Research, The Ohio State University, Columbus, OH, USA
2. ²Department of Medicine, Division of Molecular Oncology, Washington University School of Medicine, St Louis, MO, USA
3. ³Department of Medicine, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA

Correspondence: Professor K Boris-Lawrie, Department of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Goss Laboratory, Columbus, Ohio, 43210, USA. E-mail: boris-lawrie.1@osu.edu

Received 20 September 2007; Revised 25 February 2008; Accepted 18 March 2008; Published online 21 April 2008.

Abstract

JunD is a versatile AP-1 transcription factor that can activate or repress a diverse collection of target genes. Precise control of junD expression and JunD protein–protein interactions modulate tumor angiogenesis, cellular differentiation, proliferation and apoptosis. Molecular and clinical knowledge of two decades has revealed that precise JunD activity is elaborated by interrelated layers of constitutive transcriptional control, complex post-transcriptional regulation and a collection of post-translational modifications and protein–protein interactions. The stakes are high, as inappropriate JunD activity contributes to neoplastic, metabolic and viral diseases. This article deconvolutes multiple layers of control that safeguard junD gene expression and functional activity. The activity of JunD in transcriptional activation and repression is integrated into a regulatory network by which JunD exerts a pivotal role in cellular growth control. Our discussion of the JunD regulatory network integrates important open issues and posits new therapeutic targets for the neoplastic, metabolic and viral diseases associated with JunD/AP-1 expression.