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Prepublished online as a Blood First Edition Paper on October 24, 2002; DOI 10.1182/blood-2002-07-2072. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-07-2072v1 101/5/1956    most recent 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 Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Sun, Q. Articles by Chaudhary, P. M. Search for Related Content PubMed PubMed Citation Articles by Sun, Q. Articles by Chaudhary, P. M. Related Collections Neoplasia Apoptosis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 March 2003, Vol. 101, No. 5, pp. 1956-1961 NEOPLASIA The human herpes virus 8-encoded viral FLICE inhibitory protein protects against growth factor withdrawal-induced apoptosis via NF-B activation Qinmiao Sun, Hittu Matta, and Preet M. Chaudhary From the Hamon Center for Therapeutic Oncology Research and Division of Hematology-Oncology, University of Texas Southwestern Medical Center, Dallas, TX. The human herpes virus 8 (HHV8)-encoded viral FLICE (Fas-associating protein with death domain-like interleukin-1-converting enzyme) inhibitory protein (vFLIP) is believed to protect cells against death receptor-mediated apoptosis. In the present study we demonstrate that expression of HHV8 vFLIP in a growth factor-dependent TF-1 leukemia cell line protects against growth factor withdrawal-induced apoptosis. Unlike vector-expressing cells, those expressing HHV8 vFLIP maintain their mitochondrial membrane potential upon withdrawal from growth factor and also exhibit a block in the activation of caspases. The protective effect of HHV8 vFLIP is associated with its ability to activate the nuclear factor- B (NF-B) pathway and is missing in the vFLIP encoded by equine herpes virus 2 that lacks this activity. Inhibition of the NF-B pathway by IB superrepressor, lactacystin, MG132, arsenic trioxide, and phenylarsine oxide reverse the protection against growth factor withdrawal-induced apoptosis conferred by HHV8 vFLIP. HHV8 vFLIP up-regulates the expression of Bcl-xL, an antiapoptotic member of the Bcl2 family, which is a known target of the NF-B pathway. Collectively, the above results suggest that HHV8 vFLIP-induced NF-B activation may contribute to cellular transformation seen in association with HHV8 infection by preventing the apoptosis of cells destined to die because of growth factor deprivation. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F.-C. Ye, F.-C. Zhou, J.-P. Xie, T. Kang, W. Greene, K. Kuhne, X.-F. Lei, Q.-H. Li, and S.-J. Gao Kaposi's Sarcoma-Associated Herpesvirus Latent Gene vFLIP Inhibits Viral Lytic Replication through NF-{kappa}B-Mediated Suppression of the AP-1 Pathway: a Novel Mechanism of Virus Control of Latency J. Virol., May 1, 2008; 82(9): 4235 - 4249. [Abstract] [Full Text] [PDF] Y. Xu and D. Ganem Induction of chemokine production by latent Kaposi's sarcoma-associated herpesvirus infection of endothelial cells J. Gen. Virol., January 1, 2007; 88(1): 46 - 50. [Abstract] [Full Text] [PDF] C. Grossmann, S. Podgrabinska, M. Skobe, and D. Ganem Activation of NF-{kappa}B by the Latent vFLIP Gene of Kaposi's Sarcoma-Associated Herpesvirus Is Required for the Spindle Shape of Virus-Infected Endothelial Cells and Contributes to Their Proinflammatory Phenotype J. Virol., July 15, 2006; 80(14): 7179 - 7185. [Abstract] [Full Text] [PDF] M. Pearce, S. Matsumura, and A. C. Wilson Transcripts Encoding K12, v-FLIP, v-Cyclin, and the MicroRNA Cluster of Kaposi's Sarcoma-Associated Herpesvirus Originate from a Common Promoter J. Virol., November 15, 2005; 79(22): 14457 - 14464. [Abstract] [Full Text] [PDF] A. Rodriguez, N. Martinez, F. I. Camacho, E. Ruiz-Ballesteros, P. Algara, J.-F. Garcia, J. Menarguez, T. Alvaro, M. F. Fresno, F. Solano, et al. Variability in the Degree of Expression of Phosphorylated I{kappa}B{alpha} in Chronic Lymphocytic Leukemia Cases With Nodal Involvement Clin. Cancer Res., October 15, 2004; 10(20): 6796 - 6806. [Abstract] [Full Text] [PDF] L. T. Krug, V. P. Pozharskaya, Y. Yu, N. Inoue, and M. K. Offermann Inhibition of Infection and Replication of Human Herpesvirus 8 in Microvascular Endothelial Cells by Alpha Interferon and Phosphonoformic Acid J. Virol., August 1, 2004; 78(15): 8359 - 8371. [Abstract] [Full Text] [PDF] H. Matta and P. M. Chaudhary Activation of alternative NF-{kappa}B pathway by human herpes virus 8-encoded Fas-associated death domain-like IL-1{beta}-converting enzyme inhibitory protein (vFLIP) PNAS, June 22, 2004; 101(25): 9399 - 9404. [Abstract] [Full Text] [PDF] Q. Sun, S. Zachariah, and P. M. Chaudhary The Human Herpes Virus 8-Encoded Viral FLICE-inhibitory Protein Induces Cellular Transformation via NF-{kappa}B Activation J. Biol. Chem., December 26, 2003; 278(52): 52437 - 52445. [Abstract] [Full Text] [PDF] N. Field, W. Low, M. Daniels, S. Howell, L. Daviet, C. Boshoff, and M. Collins KSHV vFLIP binds to IKK-{gamma} to activate IKK J. 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