Emerging data on androgen receptor splice variants in prostate cancer

  1. Yan Dong1,2
  1. 1College of Life Sciences, Jilin University, Changchun, Jilin, China
  2. 2Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, Louisiana, USA
  1. Correspondence should be addressed to Y Dong; Email: ydong{at}tulane.edu
  1. Figure 1

    Schematic representation of the structure of AR-FL and AR-V transcripts and proteins. (A) AR gene structure with canonical exons and the cryptic exons (CE). (B) AR-FL mRNA structure showing exons encoding the N-terminal domain (NTD; exon 1), DNA-binding domain (DBD; exons 2 and 3), hinge region (part of exons 3 and 4) and ligand-binding domain (LBD; exons 5–8). AF-1, Tau1, Tau5/AF-5 and AF-2 are activation function domains. Filled triangle depicts the D-box, which mediates AR-V/AR-V, AR-V/AR-FL and AR-FL/AR-FL dimerization. (C) mRNA and protein structures of AR-Vs. AR-V-specific peptide sequences are indicated in red, and the ‘-’ in ARv56es indicates a unique junction. Inverted open triangle depicts translation stop. Drawings are not to scale. Exon 9 harbors four cryptic 3′ splicing sites, and the corresponding cryptic exons are indicated as 9a, 9b, 9c and 9d.

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