期刊
RADIATION RESEARCH
卷 161, 期 5, 页码 535-539出版社
RADIATION RESEARCH SOC
DOI: 10.1667/RR3169
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资金
- NCI NIH HHS [2R01 CA 78554, CA46592] Funding Source: Medline
Bel-X-S is a pro-apoptosis member of the Bcl2 family that has been shown to induce cell death and enhance chemosensitivity. We have investigated the effect of Bcl-X-S overexpression on radiation sensitivity. Using a tetracycline-repressible system, we found that removal of tetracycline for 16 h induced Bcl-X-S and reduced the surviving fraction of NIH 3T3 cells to 25%. However, radiation sensitivity was not significantly affected by Bcl-X-S expression; the mean inactivation doses for Bcl-X-S repressed and Bcl-X-S induced cells were 2.7 +/- 0.3 and 2.3 +/- 0.1 Gy, respectively. We conclude that Bcl-X-S induces cell death without affecting radiation sensitivity. These results suggest that mitochondrial pathways to apoptosis may not have a significant role in survival after irradiation. (C) 2004 by Radiation Research Society.
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