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Journal of Virology, January 2006, p. 281-295, Vol. 80, No. 1
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.1.281-295.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Mechanism of Telomerase Activation by v-Rel and Its Contribution to Transformation

Radmila Hrdliková, Jií Nehyba, Andrew S. Liss, and Henry R. Bose Jr.^*

Section of Molecular Genetics and Microbiology, School of Biological Sciences and Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas 78712-1095

Received 20 August 2005/ Accepted 6 October 2005

Telomerase is activated during the transformation of lymphoid cells and fibroblasts by v-Rel, the oncogenic member of the Rel/NF-B family of transcription factors. v-Rel-transformed cell lines have longer telomeres than untransformed chicken lymphoid cells and have high levels of telomerase activity. v-Rel-mediated activation of telomerase is achieved by multiple mechanisms. The expression of the gene encoding the catalytic subunit of telomerase (TERT) was directly upregulated by v-Rel. Moreover, the expression of v-Rel altered the ratio of alternatively spliced and full-length TERT transcripts in favor of the full-length forms. The activation of telomerase by v-Rel in lymphocytes was also accompanied by inactivation of nuclear inhibitors. The inhibition of telomerase activity in v-Rel-transformed cell lines led to apoptosis within 24 h. The expression of v-Rel in a macrophage cell line resulted in elevated levels of reactive oxygen species (ROS), increased telomerase activity, and increased sensitivity to telomerase inhibitors. In contrast, the ectopic expression of TERT decreased the extent of apoptosis induced by ROS. The activation of telomerase by v-Rel may, therefore, partially protect the transformed cells from apoptosis induced by ROS.

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