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Henry Bose
Mary M. Betzner Morrow Centennial Chair In Microbiology
Director, School of Biological Sciences
Email:
bose@mail.utexas.edu
Website
Main Office:
NMS 2.110
Phone:
471-5525
Alternate Office:
NMS 2.266
Alt. Phone:
471-6256
Mailing Address
The University of Texas at Austin
1 University Station A5000 - MGM
2506 Speedway
Austin ,TX 78712-1095
Research Summary
A long-standing interest of this laboratory has been to define the mechanism of transformation by the v-rel oncogene. v-Rel is the acutely transforming member of the Rel/NF-κB family of transcription factors. Transformation of cells by v-Rel results from its ability to inappropriately regulate genes normally controlled by the Rel/NF-κB family. Rel/NF-κB proteins play a central role in the regulation of genes involved in proliferation, apoptosis, and defense responses. Central to the understanding the mechanism by which v-Rel transforms cells is the identification of v-Rel target genes, which contribute to the transformed phenotype. We are currently in the process of defining how v-Rel alters the signaling pathways involved in the control of proliferation leading to cellular transformation. V-Rel also activates telomerase in avian cells by increasing the transcription of the telomerase catalytic subunit, TERT, and by reducing the expression of alternatively spliced TERT isoforms that fail to encode functional molecules. The most abundant protein coding isoforms expressed in Rel transformed cells induces cell proliferation in the absence of telomerase activity. This is the first TERT isoform identified with the non-telomerase proliferative functions separated from the telomerase activity. We have recently isolated a novel human TERT isoform which also stimulates cell proliferation in the absences of telomerase activity. This variant is expressed in cells of rapidly dividing tissue and some human tumors. We are defining whether this novel alternatively spiced variant processes other non-canonical functions of telomerase, how it is regulated and stimulates cell proliferation and whether its expression correlates with specific types of human cancer.
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