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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >RESISTANCE TO APOPTOSIS IN CTLL-2 CELLS CONSTITUTIVELY EXPRESSING C-MYB IS ASSOCIATED WITH INDUCTION OF BCL-2 EXPRESSION AND MYB-DEPENDENT REGULATION OF BCL-2 PROMOTER ACTIVITY
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RESISTANCE TO APOPTOSIS IN CTLL-2 CELLS CONSTITUTIVELY EXPRESSING C-MYB IS ASSOCIATED WITH INDUCTION OF BCL-2 EXPRESSION AND MYB-DEPENDENT REGULATION OF BCL-2 PROMOTER ACTIVITY

机译：组成型表达C-MYB的CTLL-2细胞对凋亡的抵抗与BCL-2表达的诱导和BCL-2启动子活性的MYB依赖性调节相关

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c-Myb, the cellular homologue of the transforming gene of the avian myeloblastosis virus, is preferentially expressed in all hematopoietic lineages, including T and B lymphocyte lineages, In T lymphocytes, c-Myb expression appears to be required for cell cycle progression and proliferation, To further investigate the role of c-Myb in T cell proliferation and survival, interleukin (IL) 2-dependent CTLL-2 cells were transfected with a constitutively active c-myb or with a c-myb antisense construct able to down-regulate endogenous Myb levels, and the transfectants were assessed for proliferation and survival in low concentrations of IL-2 and for susceptibility to dexamethasone-induced apoptosis, Compared with control cells, CTLL-2 cells constitutively expressing c-Myb proliferate in low concentrations of IL-2 and are less susceptible to apoptosis induced bq IL-2 deprivation or treatment with dexamethasone. In contrast, cells transfected with an antisense c-myb construct do not proliferate in Low concentrations of IL-2 and undergo apoptosis upon IL-2 deprivation or dexamethasone treatment more rapidly than parental cells, Overexpression of c-Myb was accompanied by up-regulation of BCL-2 expression, In transient transfection assays, the murine bcl-2 promoter was efficiently transactivated by c-Myb, but such effect was observed also in cells transfected with a DNA binding-deficient c-myb construct, Moreover, in gel retardation assays, a 38-bp oligomer in the shortest bcl-2 promoter segment regulated by c-Myb formed a specific complex with nuclear extracts from c-Myb transfected CTLL-2 cells, Thus, these results strongly suggest that c-Myb? in addition to regulating T cell proliferation, protects T lymphocytes from apoptosis by induction of BCL-2 expression, which involves a c-Myb-dependent mechanism of promoter regulation. [References: 39]
机译：c-Myb是禽成纤维细胞病病毒转化基因的细胞同源物，在所有造血谱系中都优先表达，包括T和B淋巴细胞谱系。在T淋巴细胞中，c-Myb表达似乎是细胞周期进程和增殖所必需的，为了进一步研究c-Myb在T细胞增殖和存活中的作用，将白介素（IL）2依赖性CTLL-2细胞用组成型活性c-myb或能够下调c-myb反义构建体转染内源性Myb水平和转染子在低浓度IL-2下的增殖和存活率以及地塞米松诱导的细胞凋亡的敏感性进行了评估。与对照细胞相比，组成型表达c-Myb的CTLL-2细胞在低浓度IL-下增殖2，并且不易受凋亡诱导的bq IL-2剥夺或地塞米松治疗。相反，用反义c-myb构建体转染的细胞在低浓度的IL-2中不增殖，并且在IL-2被剥夺或地塞米松处理后比亲代细胞更快地凋亡，c-Myb的过表达伴随上调BCL-2表达的变化，在瞬时转染实验中，鼠bcl-2启动子被c-Myb有效地激活，但是在用DNA结合缺陷的c-myb构建体转染的细胞中也观察到了这种作用，此外，在凝胶阻滞中在实验中，由c-Myb调节的最短bcl-2启动子片段中的38 bp寡聚物与c-Myb转染的CTLL-2细胞的核提取物形成了特定的复合物，因此，这些结果强烈表明c-Myb？除了调节T细胞增殖外，还通过诱导BCL-2表达来保护T淋巴细胞免于凋亡，这涉及c-Myb依赖的启动子调节机制。 [参考：39]

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