| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
1 Department of Biochemistry and Molecular Biology, 2 Center for Genomics Research, Wright State University, Dayton, Ohio; and 3 Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, New Hampshire
Requests for reprints: Madhavi P. Kadakia, Department of Biochemistry and Molecular Biology, Wright State University, Dayton, OH 45435. Phone: 937-775-2339; Fax: 937-775-3730. E-mail: madhavi.kadakia{at}wright.edu
p63 and p73 are members of the p53 protein family and have been shown to play an important role in cell death, development, and tumorigenesis. In particular, p63 has been shown to be involved in the maintenance of epidermal stem cells and in the stratification of the epidermis. Sonic Hedgehog (Shh) is a morphogen that has also been implicated to play a role in epithelial stem cell proliferation and in the development of organs. Recently, Shh has also been shown to play an important role in the progression of a variety of cancers. In this report, we show that p63 and p73 but not p53 overexpression induces Shh expression. In particular, p63
and p63ß (both TA and 
N isoforms) and TAp73ß isoform induce Shh. Expression of Shh was found to be significantly reduced in mouse embryo fibroblasts obtained from p63–/– mice. The naturally occurring p63 mutant TAp63(R279H) and the tumor suppressor protein p14ARF inhibited the TAp63-mediated transactivation of Shh. The region –228 to –102 bp of Shh promoter was found to be responsive to TAp63-induced transactivation and TAp63 binds to regions within the Shh promoter in vivo. The results presented in this study implicate p63 in the regulation of the Shh signaling pathway. (Mol Cancer Res 2006;4(10):759–68)
This article has been cited by other articles:
|
|
 |
|
  T. Rinne, S. E. Clements, E. Lamme, P. H.G. Duijf, E. Bolat, R. Meijer, H. Scheffer, E. Rosser, T. Y. Tan, J. A. McGrath, et al. A novel translation re-initiation mechanism for the p63 gene revealed by amino-terminal truncating mutations in Rapp-Hodgkin/Hay-Wells-like syndromes Hum. Mol. Genet., July 1, 2008; 17(13): 1968 - 1977. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Sasaki, Y. Oshima, R. Koyama, R. Maruyama, H. Akashi, H. Mita, M. Toyota, Y. Shinomura, K. Imai, and T. Tokino Identification of Flotillin-2, a Major Protein on Lipid Rafts, as a Novel Target of p53 Family Members Mol. Cancer Res., March 1, 2008; 6(3): 395 - 406. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Xin, R. U. Lukacs, D. A. Lawson, D. Cheng, and O. N. Witte Self-Renewal and Multilineage Differentiation In Vitro from Murine Prostate Stem Cells Stem Cells, November 1, 2007; 25(11): 2760 - 2769. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kommagani, V. Payal, and M. P. Kadakia Differential Regulation of Vitamin D Receptor (VDR) by the p53 Family: p73-DEPENDENT INDUCTION OF VDR UPON DNA DAMAGE J. Biol. Chem., October 12, 2007; 282(41): 29847 - 29854. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |
