...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Mad1 expression in the absence of differentiation: effect of cAMP on the B-lymphoid cell line Reh.
【24h】

Mad1 expression in the absence of differentiation: effect of cAMP on the B-lymphoid cell line Reh.

机译：Mad1表达式没有分化:营地在b淋巴细胞系盐土的效果。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The protein Mad1 heterodimerizes with Max to form an E-box binding complex able to interfere with the transcriptional and transforming activities of c-Myc. Downregulation of c-Myc accompanied by induction of Mad1 upon differentiation has fueled the notion that Mad1 may play a role in the cessation of proliferation associated with the differentiation process. Since studies on Mad1 expression have so far been limited to cells undergoing differentiation, it was of interest to examine Mad1 expression in a cell system unable to differentiate. To do so, we utilized the leukemia-derived B-precursor cell line, Reh, and studied the expressions of Mad1, c-Myc, Mxil, and Max during cAMP-mediated growth inhibition of these cells. Thus, the adenylate cyclase activator forskolin induced growth inhibition of the cells in the G1 phase of the cell cycle. This growth inhibition was associated with transient increased expression of Mad1 concomitant with transient downregulation of c-Myc. The Mad1 protein levels essentially paralleled those of mRNA, with peak levels at 4 h of forskolin treatment. By coimmunoprecipitation we detected increased binding of Mad1 to Max in forskolin-treated cells, indicating that the changes in Mad1 protein levels had functional implications. By continually treating Reh cells with forskolin for 72 h, we observed a sustained elevated expression of Mad1 concomitant with downregulated c-Myc expression, still without changing the differentiation profile of the Reh cells. Interestingly, we showed that other known cell cycle regulatory proteins also were transiently regulated by forskolin. To this extent, following forskolin treatment of Reh cells, cyclin E-cdk2 activity was transiently reduced concomitant with dephosphorylation of pRB. We suggest that the early changes in Mad1 and the cell cycle regulatory proteins initiate a chain of events resulting in permanent growth arrest. Thus, the increased expression of Mad1 in the absence of differentiation indicates that Mad1 expression in Reh cells is linked to growth arrest per se.
机译：与马克斯蛋白质Mad1二聚化形成一个E-box结合复杂的干扰转录和转换活动原癌基因。Mad1诱导分化引发认为Mad1可能发挥的作用停止增殖相关分化的过程。迄今为止,表达仅限于细胞进行分化,这是感兴趣的不能检查Mad1表达在细胞系统来区分。leukemia-derived B-precursor细胞系、盐土和研究Mad1的表情,原癌基因,Mxil,马克斯在cAMP-mediated抑制增长这些细胞。活化剂forskolin诱导生长抑制细胞的细胞周期G1期。生长抑制瞬态增加表达Mad1相伴原癌基因的差别瞬态对这些。蛋白质含量基本上是平行的信使rna, 4 h forskolin最高水平治疗。绑定Mad1马克斯在增加forskolin-treated细胞,表明Mad1蛋白质水平变化功能的影响。与forskolin 72 h,我们观察到的持续高表达Mad1相伴表达下调原癌基因表达,还是没有改变分化的盐土细胞。细胞周期调控蛋白也暂时性的由forskolin监管。程度上,之后forskolin盐土细胞,细胞周期蛋白E-cdk2活动是暂时性的减少相伴的去磷酸化复审委员会。和细胞周期调控蛋白启动一系列事件导致永久性的增长逮捕。分化表明的缺失Mad1盐土细胞表达与增长为自己的。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号