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Prepublished online as a Blood First Edition Paper on November 7, 2002; DOI 10.1182/blood-2002-04-1103. This Article Full Text (PDF) All Versions of this Article: 2002-04-1103v1 101/5/1928    most recent Alert me when this article is cited Alert me if a correction is posted 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 Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Porter, L. A Articles by Lee, J. M Search for Related Content PubMed PubMed Citation Articles by Porter, L. A Articles by Lee, J. M Social Bookmarking                   What's this? Submitted April 11, 2002 Accepted October 17, 2002 Nuclear localization of cyclin B1 regulates DNA damage-induced apoptosis Lisa A Porter, I Howard Cukier, and Jonathan M Lee* Hamilton Regional Cancer Center, Hamilton, ON, Canada Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada * Corresponding author; email: jonathan.lee{at}hrcc.on.ca. Some cells undergo apoptosis in response to DNA damage, while others do not. To understand the biochemical pathways controlling this differential response, we have studied the intracellular localization of cyclin B1 in cell types sensitive or resistant to DNA damage-induced apoptosis. We find that cyclin B1 protein accumulates in the nucleus of cells that are sensitive to -radiation-induced apoptosis (thymocytes, lymphoid cell lines), but remains cytoplasmic in apoptosis-resistant cells (primary and transformed fibroblasts). Treatment of both cell types with Leptomycin B, an inhibitor of Crm1-dependent cyclin B1 nuclear export, induces apoptosis. Furthermore, ectopic expression of cyclin B1-5xE, a protein that preferentially localizes to the nucleus, is sufficient to trigger apoptosis. Conversely, expression of cyclin B1-5xA, a predominantly cytoplasmic protein, fails to induce apoptosis. This suggests that nuclear accumulation is necessary for cyclin B1-dependent apoptosis. Our observations are consistent with the idea that localization of cyclin B1 is among the factors determining the cellular decision to undergo apoptosis in response to DNA damage. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. W. Chan, C. J. Lim, L. S. Loo, Y. F. Chong, C. Huang, and W. Hong TEADs Mediate Nuclear Retention of TAZ to Promote Oncogenic Transformation J. Biol. Chem., May 22, 2009; 284(21): 14347 - 14358. [Abstract] [Full Text] [PDF] G. Natarajan, S. Ramalingam, I. Ramachandran, R. May, L. Queimado, C. W. Houchen, and S. Anant CUGBP2 downregulation by prostaglandin E2 protects colon cancer cells from radiation-induced mitotic catastrophe Am J Physiol Gastrointest Liver Physiol, May 1, 2008; 294(5): G1235 - G1244. [Abstract] [Full Text] [PDF] H. Jiang, S. Luo, and H. Li Cdk5 Activator-binding Protein C53 Regulates Apoptosis Induced by Genotoxic Stress via Modulating the G2/M DNA Damage Checkpoint J. Biol. Chem., May 27, 2005; 280(21): 20651 - 20659. [Abstract] [Full Text] [PDF] B. Li, M. Nair, D. R. Mackay, V. Bilanchone, M. Hu, M. Fallahi, H. Song, Q. Dai, P. E. Cohen, and X. Dai Ovol1 regulates meiotic pachytene progression during spermatogenesis by repressing Id2 expression Development, March 15, 2005; 132(6): 1463 - 1473. [Abstract] [Full Text] [PDF] S. Wen, C. P. Felley, H. Bouzourene, M. Reimers, P. Michetti, and Q. Pan-Hammarstrom Inflammatory Gene Profiles in Gastric Mucosa during Helicobacter pylori Infection in Humans J. Immunol., February 15, 2004; 172(4): 2595 - 2606. [Abstract] [Full Text] [PDF]

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