@misc{oai:repo.qst.go.jp:00069157,
 author = {Sudo, Makoto and Nakayama, Fumiaki and Watanabe, Keiko and Hachiya, Misao and Akashi, Makoto and 須藤 誠 and 中山 文明 and 渡辺 恵子 and 蜂谷 みさを and 明石 真言},
 month = {Dec},
 note = {Irradiation causes various types of cell damage including DNA, stimulates the generation of reactive oxygen species (ROS), and activates multiple signal pathways in cells.  Previously, we showed that irradiation markedly increased the tumor necrosis factor alpha (TNFalpha) production in cells.  TNFalpha has both apoptotic and anti-apoptotic properties depending on the activation of signaling pathways.  To study the role of TNFalpha in irradiation, human T cell line Jurkat cells were transfected with TNFalpha short interfering (si) RNA (siRNA).  Studies of competitive PCR showed that an increased level of TNFalpha mRNA was observed immediately after 10 Gy irradiation in control cells; the level reached a maximum at 30 min and then decreased gradually.  However, the knock-down of TNFalpha using siRNA significantly abolished the irradiation-induced accumulation of TNFalpha mRNA.  We also investigated the mRNA levels of Bax, Bcl-2, and Bcl-XL. Levels of Bcl-2 and Bcl-XL mRNA were similar in control cells and TNFalpha knock-down(k/d) cells.  However, the level of Bax mRNA was apparently higher in TNFalpha k/d cells than control cells but irradiation failed to increase the level in both cell lines.  On the other hand, staining with Annexin-V and detection of DNA fragmentation showed that irradiation at a dose of 10 Gy induced apoptosis more frequently in the control cells than TNFalpha k/d cells.  These results indicate that irradiation induces apoptosis through a pathway requiring TNFalpha production in these cells.  Our result also suggest that apoptosis by irradiation occurs independent of the Bax expression.  Further studies on the mechanisms are in progress., 日本分子生物2006フォーラム},
 title = {Endogenous production of TNFalpha regulates apoptosis by irradiation in a human T cell line Jurkat},
 year = {2006}
}