摘要
蛋氨酸 adenosyltransferase II (地席 II ) 是在细胞的新陈代谢的关键酶并且从 L 蛋氨酸和 ATP 催化 S-adenosylmethionine (一样) 的形成。正常休息 T 淋巴细胞举办最小的地席 II 活动，而白血病的房间显著地显示出的激活的增殖的 T 淋巴细胞和转变 T 提高了地席 II 活动。这个工作被执行在白血病的 T 房间的幸存检验地席 II 活动和一样的生合成的角色。在一样的层次的地席 II 和结果的减少的抑制提高了 FasL mRNA 和蛋白质的表示，并且导致了圆盘(导致发信号的建筑群的死亡) 有 FADD (联系船边交货的死亡域) 和 procaspase-8 招募的形成，以及 caspase-8 激活的伴随物增加和在 c 扭动的减少铺平。开始船边交货的发信号由地席 II 抑制导致了被观察经由出价劈开连接到 mitochondrial 小径并且最终在这些房间导致增加的 caspase-3 激活和 DNA 破碎。而且，堵住地席 2A mRNA 表示，它编码地席 II 的催化子单元，用一条小介入的 RNA 途径提高了 FasL 表示和房间死亡，验证在 T 白血病的房间的幸存的地席 II 活动的必要性质。
Methionine adenosyltransferase Ⅱ（MAT Ⅱ） is a key enzyme in cellular metabolism and catalyzes the formation of S-adenosylmethionine （SAMe） from L-methionine and ATE Normal resting T lymphocytes have minimal MAT Ⅱ activity, whereas activated proliferating T lymphocytes and transformed T leukemic cells show significantly enhanced MAT Ⅱ activity. This work was carried out to examine the role of MAT Ⅱ activity and SAMe biosynthesis in the survival of leukemic T cells. Inhibition of MAT Ⅱ and the resultant decrease in SAMe levels enhanced expression of FasL mRNA and protein, and induced DISC （Death Inducing Signaling Complex） formation with FADD （Fasassociated Death Domain） and procaspase-8 recruitment, as well as concomitant increase in caspase-8 activation and decrease in c-FLIPs levels. Fas-initiated signaling induced by MAT Ⅱ inhibition was observed to link to the mitochondrial pathway via Bid cleavage and to ultimately lead to increased caspase-3 activation and DNA fragmentation in these cells. Furthermore, blocking MAT 2A mRNA expression, which encodes the catalytic subunits of MAT Ⅱ, using a small-interfering RNA approach enhanced FasL expression and cell death, validating the essential nature of MAT Ⅱ activity in the survival of T leukemic cells.
