INTERLEUKIN-2 INDUCTION OF T-CELL G1 PROGRESSION AND C-MYB EXPRESSION
INTERLEUKIN-2 INDUCTION OF T-CELL G1 PROGRESSION AND C-MYB EXPRESSION
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DOI：
10.1126/science.3523754
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发表时间：
1986-07-11
期刊：
影响因子：
56.9
通讯作者：
SMITH, KA
中科院分区：
文献类型：
--
作者：
STERN, JB;SMITH, KA
在确定细胞增殖的生化机制的研究中，同步T细胞被用作细胞生长控制的模型。通过代谢和形态学标准，发现t细胞抗原受体的激活使细胞对白细胞介素-2 （IL-2）产生反应，但没有使它们通过细胞周期。相反，IL-2刺激G1进展到S期，或淋巴细胞成母转化。在il -2促进的G1进程中，细胞原癌基因c-myb的表达被短暂地诱导为基础水平的6 - 7倍，最高水平出现在G1的中点。
In studies to determine the biochemical mechanisms responsible for cell proliferation, synchronized T cells were used as a model for cellular growth control. By metabolic and morphologic criteria, it was found that activation of the T-cell antigen receptor rendered the cells responsive to interleukin-2 (IL-2), but did not move them through the cell cycle. Instead, IL-2 stimulated G1 progression to S phase, or lymphocyte blastic transformation. During IL-2-promoted G1 progression, expression of the cellular proto-oncogene c-myb was induced transiently at six to seven times basal levels, maximal levels occurring at the midpoint of G1.