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Prostate Cancer
Volume 2014 (2014), Article ID 129582, 9 pages
Research Article

Role of p73 Dinucleotide Polymorphism in Prostate Cancer and p73 Protein Isoform Balance

1Department of Chemistry, Biochemistry & Physics, University of Tampa, Tampa, FL 33606, USA
2Department of Biostatistics, Moffitt Cancer Center, Tampa, FL 33612, USA
3Department of Cancer Epidemiology, Moffitt Cancer Center, 12902 Magnolia Drive, Tampa, FL 33612, USA
4Department of Molecular Oncology, Moffitt Cancer Center, Tampa, FL 33612, USA
5Department of Anatomic Pathology, Moffitt Cancer Center, Tampa, FL 33612, USA
6Genitourinary Program, James Haley VA Hospital, Tampa, FL 33612, USA
7Genitourinary Program, Moffitt Cancer Center, Tampa, FL 33612, USA

Received 10 March 2014; Revised 21 May 2014; Accepted 22 May 2014; Published 6 July 2014

Academic Editor: Scott E. Eggener

Copyright © 2014 L. Michael Carastro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplement Figure 1. p73 Gene and N-terminal isoforms of p73 protein. The structure of the p73 gene is depicted, including the p73 gene exons (black filled boxes for all exons, except exon 1 and exon 4 are labeled unfilled boxes), introns (lines connecting boxes), and p73 gene promotes (P1 & P2). The approximate position of the p73 dinucleotide polymorphism (p73 DNP) in exon 2 is indicated. The two major N-terminal protein isoforms of p73, TAp73 and ΔNp73, are depicted (below the p73 gene), including the major functional domains (TA = transactivation domain; DBD = DNA-binding domain; OD = oligomerization domain). The TAp73 form includes exons 1 through 3, which are absent in the ΔNp73 isoforms.

  1. Supplementary Material