QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Research Data Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Teodoro, J. G. Articles by Green, M. R. Search for Related Content PubMed PubMed Citation Articles by Teodoro, J. G. Articles by Green, M. R. Social Bookmarking                   What's this?

RESEARCH COMMUNICATION

The viral protein Apoptin associates with the anaphase-promoting complex to induce G2/M arrest and apoptosis in the absence of p53

Howard Hughes Medical Institute, Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA

The chicken anemia virus protein Apoptin induces apoptosis in the absence of p53 by a mechanism that remains to be elucidated. Here we show that in transformed cells, Apoptin is associated with APC1, a subunit of the anaphase-promoting complex/cyclosome (APC/C). We demonstrate that Apoptin expression, or depletion of APC1 by RNA interference, inhibits APC/C function in p53 null cells, resulting in G2/M arrest and apoptosis. Our results explain the ability of Apoptin to induce apoptosis in the absence of p53 and suggest that the APC/C is an attractive target for anticancer drug development.

[Keywords: Apoptin; apoptosis; G2/M arrest; anaphase-promoting complex/cyclosome; p53-independent; RNA interference]

Received February 25, 2004; revised version accepted June 21, 2004.

Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1198404.

¹ These authors contributed equally to this work.

² Corresponding author.
E-MAIL michael.green{at}umassmed.edu; FAX (508) 856-5473.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				K. Tran, J. A. Mahr, J. Choi, J. G. Teodoro, M. R. Green, and D. H. Spector Accumulation of Substrates of the Anaphase-Promoting Complex (APC) during Human Cytomegalovirus Infection Is Associated with the Phosphorylation of Cdh1 and the Dissociation and Relocalization of APC Subunits J. Virol., January 1, 2008; 82(1): 529 - 537. [Abstract] [Full Text] [PDF]

				D. W. Heilman, J. G. Teodoro, and M. R. Green Apoptin Nucleocytoplasmic Shuttling Is Required for Cell Type-Specific Localization, Apoptosis, and Recruitment of the Anaphase-Promoting Complex/Cyclosome to PML Bodies. J. Virol., August 1, 2006; 80(15): 7535 - 7545. [Abstract] [Full Text] [PDF]

				S. Blachon, S. Bellanger, C. Demeret, and F. Thierry Nucleo-cytoplasmic Shuttling of High Risk Human Papillomavirus E2 Proteins Induces Apoptosis J. Biol. Chem., October 28, 2005; 280(43): 36088 - 36098. [Abstract] [Full Text] [PDF]

				S. Maddika, E. P. Booy, D. Johar, S. B. Gibson, S. Ghavami, and M. Los Cancer-specific toxicity of apoptin is independent of death receptors but involves the loss of mitochondrial membrane potential and the release of mitochondrial cell-death mediators by a Nur77-dependent pathway J. Cell Sci., October 1, 2005; 118(19): 4485 - 4493. [Abstract] [Full Text] [PDF]