Nucleic Acids Research Advance Access originally published online on October 5, 2006
Nucleic Acids Research 2006 34(19):5603-5612; doi:10.1093/nar/gkl619
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Nucleic Acids Research, 2006, Vol. 34, No. 19 5603-5612
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Expression of C-terminal deleted p53 isoforms in neuroblastoma
1 Centre National de Recherche Scientifique UMR 8126 2 Centre National de Recherche Scientifique UMR 8125 3 Département de Biologie et Pathologie Médicales, Institut Gustave Roussy 94805 Villejuif, France 4 Laboratoire de Biochimie, Hôpital Saint-Louis 75010 Paris, France 5 Centre National de Recherche Scientifique UPR 9045, Institut André Lwoff 94801 Villejuif, France
*To whom correspondence should be addressed. Tel: +33 1 42 11 48 53; Fax: +33 1 42 11 54 94; Email: sdouc{at}igr.fr
*Correspondence may also be addressed to Evelyne May. Tel: +33 1 49 58 33 50; Fax: +33 1 49 58 33 68; Email: emay{at}vjf.cnrs.fr
Received May 25, 2006. Accepted August 8, 2006.
The tumor suppressor gene, p53, is rarely mutated in neuroblastomas (NB) at the time of diagnosis, but its dysfunction could result from a nonfunctional conformation or cytoplasmic sequestration of the wild-type p53 protein. However, p53 mutation, when it occurs, is found in NB tumors with drug resistance acquired over the course of chemotherapy. As yet, no study has been devoted to the function of the specific p53 mutants identified in NB cells. This study includes characterization and functional analysis of p53 expressed in eight cell lines: three wild-type cell lines and five cell lines harboring mutations. We identified two transcription-inactive p53 variants truncated in the C-terminus, one of which corresponded to the p53ß isoform recently identified in normal tissue by Bourdon et al. [J. C. Bourdon, K. Fernandes, F. Murray-Zmijewski, G. Liu, A. Diot, D. P. Xirodimas, M. K. Saville and D. P. Lane (2005) Genes Dev., 19, 2122–2137]. Our results show, for the first time, that the p53ß isoform is the only p53 species to be endogenously expressed in the human NB cell line SK-N-AS, suggesting that the C-terminus truncated p53 isoforms may play an important role in NB tumor development.
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors
GenBank accession nos KO3199 (mRNA) and X54156 [GenBank] (HSP53G)
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