@misc{oai:repo.qst.go.jp:00069247,
 author = {Sudo, Makoto and Sai, Sei and Akashi, Makoto and 須藤 誠 and 崔 星 and 明石 真言},
 month = {Dec},
 note = {Tumor necrosis factor alpha (TNFalpha) is one of mediators of apoptosis as well as inflammation and immunity, and is produced upon radiation exposure.  TNFalpha is a unique proinflammatory cytokine whose signaling pathways are linked to both anti- and pro-apoptotic responses in many cell types.  To better understand the role of TNFalpha after high dose radiation, we have knocked-down TNFalpha by siRNA and examined changes of apoptosis-related proteins in human Jurkat T leukemia cells.  Jurkat cells were transfected with TNFalpha-specific siRNA.  Both control and TNFalpha-siRNA transfected cells were pretreated with an inhibitor of MEK, p38 MAPK or PI3K, and were irradiated with X-ray at a dose of 10Gy.  DNA fragmentation analysis showed that transfection with TNFalpha- siRNA significantly blocked radiation-induced apoptosis.  Western blot analysis showed that radiation induced phosphorylation of both ERK and p38 MAPK, which was further enhanced in TNFalpha- siRNA transfected cells even in the presence of a specific inhibitor of MEK or p38 MAPK.  Phosphorylation of Akt was also induced in TNFalpha-siRNA transfected cells after irradiation.  Radiation induced Bax expression and caspase-3 activation in the control cells, and transfection with TNFalpha-siRNA suppressed caspase-3 activation and up-regulated expression of Bcl-2 and Bcl-xL, whereas further enhanced Bax expression was observed.  In conclusion, radiation induces apoptosis through activation of MEK/p38 MAPK and caspase/mitochondria pathways requiring TNFalpha.  Further studies on the mechanisms are in progress., 第30回日本分子生物学会年会･第80回日本生化学会大会合同大会},
 title = {Radiation induces apoptosis through endogenous Tumor Necrosis Factor alpha via activation of MEK/p38 MAPK and mitochondria/caspases pathways in Jurkat T leukemia cells},
 year = {2007}
}