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New binding target for oncogenic viral protein

"These proteins are also some of the most broadly acting cellular oncogenes, and include cyclin E, c-Myc, Notch, and c-Jun," noted Dr. Clurman. "When Fbw7 is mutated in cancers, deregulation of these oncogenic Fbw7 targets is thought to contribute to cancer. SV40 T antigen contains a motif that mimics the destruction signal found in these proteins." However, unlike the other substrates recognized by Fbw7, T antigen is not destroyed by the cell.

Drs. Clurman and Welcker suspect that by acting as a decoy and binding to Fbw7, T antigen protects cellular Fbw7 targets that facilitate viral replication and tumorigenesis.

"I think this work underlines the importance of Fbw7 as an emerging tumor suppressor and the consequences of its loss in tumors," Dr. Welcker emphasized.

"The study of DNA tumors viruses has been an extremely important tool in understanding the cellular pathways that regulate cell division and are disrupted in cancer. Understanding the mechanisms through which these viruses interact with the cellular machinery that regulates cell division may lead to new insights into the pathways that cause cancer. This is an important step to designing new cancer treatment strategies that target these pathways," concluded Dr. Clurman.


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Contact: Nicole Kresge
nkresge@asbmb.org
301-634-7415
American Society for Biochemistry and Molecular Biology
25-Feb-2005


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