...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >BETA3, a novel helix-loop-helix protein, can act as a negative regulator of BETA2 and MyoD-responsive genes.
【24h】

BETA3, a novel helix-loop-helix protein, can act as a negative regulator of BETA2 and MyoD-responsive genes.

机译：BETA3是一种新型的螺旋-环-螺旋蛋白，可以作为BETA2和MyoD响应基因的负调节剂。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Using degenerate PCR cloning we have identified a novel basic helix-loop-helix (bHLH) transcription factor, BETA3, from a hamster insulin tumor (HIT) cell cDNA library. Sequence analysis revealed that this factor belongs to the class B bHLH family and has the highest degree of homology with another bHLH transcription factor recently isolated in our laboratory, BETA2 (neuroD) (J. E. Lee, S. M. Hollenberg, L. Snider, D. L. Turner, N. Lipnick, and H. Weintraub, Science 268:836-844, 1995; F. J. Naya, C. M. M. Stellrecht, and M.-J. Tsai, Genes Dev. 8:1009-1019, 1995). BETA2 is a brain- and pancreatic-islet-specific bHLH transcription factor and is largely responsible for the tissue-specific expression of the insulin gene. BETA3 was found to be tissue restricted, with the highest levels of expression in HIT, lung, kidney, and brain cells. Surprisingly, despite the homology between BETA2 and BETA3 and its intact basic region, BETA3 is unable to bind the insulin E box in bandshift analysis as a homodimer or as a heterodimer with the class A bHLH factors E12, E47, or BETA1. Instead, BETA3 inhibited both the E47 homodimer and the E47/BETA2 heterodimer binding to the insulin E box. In addition, BETA3 greatly repressed the BETA2/E47 induction of the insulin enhancer in HIT cells as well as the MyoD/E47 induction of a muscle-specific E box in the myoblast cell line C2C12. In contrast, expression of BETA3 had no significant effect on the GAL4-VP16 transcriptional activity. Immunoprecipitation analysis demonstrates that the mechanism of repression is via direct protein-protein interaction, presumably by heterodimerization between BETA3 and class A bHLH factors.
机译：使用简并PCR克隆，我们从仓鼠胰岛素肿瘤（HIT）细胞cDNA文库中鉴定了一种新型的基本螺旋-环-螺旋（bHLH）转录因子BETA3。序列分析表明，该因子属于B类bHLH家族，与最近在我们实验室分离的另一种bHLH转录因子BETA2（neuroD）具有最高的同源性（JE Lee，SM Hollenberg，L。Snider，DL Turner，N Lipnick and H.Weintraub，Science 268：836-844，1995; FJ Naya，CMM Stellrecht，和M.-T. Tsai，Genes Dev。8：1009-1019，1995）。 BETA2是脑和胰岛特异性bHLH转录因子，在很大程度上负责胰岛素基因的组织特异性表达。发现BETA3受组织限制，在HIT，肺，肾和脑细胞中具有最高水平的表达。出乎意料的是，尽管BETA2和BETA3及其完整的基本区域之间具有同源性，但BETA3在带移分析中无法与A类bHLH因子E12，E47或BETA1的同二聚体或异二聚体结合胰岛素E box。相反，BETA3抑制了E47同二聚体和E47 / BETA2异二聚体与胰岛素E盒的结合。此外，BETA3大大抑制了HIT细胞中胰岛素增强剂的BETA2 / E47诱导以及成肌细胞C2C12细胞中肌肉特异性E盒的MyoD / E47诱导。相反，BETA3的表达对GAL4-VP16转录活性没有明显影响。免疫沉淀分析表明，抑制的机制是通过直接的蛋白质-蛋白质相互作用，大概是通过BETA3与A类bHLH因子之间的异源二聚作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
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