Trends Mol Med. 2006; 12:177-185.
E2F1-related apoptosis: turning killers into therapeutics.
Stanelle J, Pützer BM.
The cellular transcription factor E2F1 is part of an anti-tumor safeguard mechanism: it engages cell-death pathways either alone or in cooperation with p53 to protect organisms from the development of tumors. E2F1 activates downstream factors, which in turn produce secondary changes in gene expression that trigger apoptosis. Although the mechanisms are incompletely understood, several studies have demonstrated that E2F1 is involved in many different aspects of programmed cell death depending on the cellular background. Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.
Contact
Institute of Experimental Gene Therapy and Cancer Research
Core-Facility Viral Vector & Genome-Editing Technologies
Biomedical Research Center
Schillingallee 69
D-18057 Rostock
Office
Ingrid Winkler
(+49) 381 494-5066(+49) 381 494-5062
ingrid.winkler@med.uni-rostock.de
Department Life, Light & Matter
Research Building LL&M
Albert-Einstein-Str. 25
D-18059 Rostock
Research Building LL&M
Albert-Einstein-Str. 25
D-18059 Rostock
