Multiple facets of junD gene expression are atypical among AP-1 family members

被引:106
|
作者
Hernandez, J. M.
Floyd, D. H. [2 ]
Weilbaecher, K. N. [2 ]
Green, P. L. [3 ]
Boris-Lawrie, K. [1 ,3 ]
机构
[1] Ohio State Univ, Dept Vet Biosci, Goss Lab, Columbus, OH 43210 USA
[2] Washington Univ, Sch Med, Dept Med, Div Mol Oncol, St Louis, MO 63110 USA
[3] Ohio State Univ, Ctr Comprehens Canc, Dept Med, Columbus, OH 43210 USA
关键词
JunD; AP-1; RNA helicase A and post-transcriptional control element; HTLV-1; cancer; heart failure;
D O I
10.1038/onc.2008.120
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 modi. cations 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.
引用
收藏
页码:4757 / 4767
页数:11
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