• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Pigment cell research >Expression of gp100 and CDK2 in melanoma cells is not co-regulated by a shared promoter region
【24h】

Expression of gp100 and CDK2 in melanoma cells is not co-regulated by a shared promoter region

机译：黑色素瘤细胞中gp100和CDK2的表达不受共享启动子区域的共同调控

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

Expression of the pigmentation-associated gene PMel17 is regulated by a 1 kB promoter region shared between the PMel17 and CDK2 genes. The encoded melanosomal glycoprotein gp100 and the cell cycle regulatory protein CDK2 are transcribed in opposite directions. Luciferase reporter constructs were generated for subregions of the promoter containing 0, 1, 2 or 3 putative binding sites for transcription factors with basic helix-loop-helix (bHLH) motifs. The potential contribution of bHLH transcription factor microphthalmia transcription factor (MITF) to promoter activity was investigated by re-introducing microphthalmia into melanoma cells lacking expression. A bi-directional reporter construct was generated to investigate potential co-regulation of gp100 and CDK2 transcription. Promoter activity was assessed in presence and absence of phorbol ester tetradecanoyl phorbol 13-acetate (TPA). FACS analysis and immunohistology served to evaluate co-regulation of gp100 and CDK2 expression at the protein level. The full-length promoter, including a consensus binding site for MITF was found to contain sequences that suppressed gp100 expression. Introduction of MITF into non-expressing 1123 melanoma cells did not restore gp100 expression levels. A lack of coregulation for gp100 and CDK2 as suggested by immunostaining was supported by findings of dissimilar expression regulation by TPA for either gene. The current study provides insight into transcriptional regulation of the PMel17 and CDK2 genes, important to identify strategies for modulating expression of gp100 and CDK2 proteins by melanoma cells.
机译：色素沉着相关基因PMel17的表达受PMel17和CDK2基因之间共有的1 kB启动子区域调控。编码的黑素体糖蛋白gp100和细胞周期调节蛋白CDK2沿相反方向转录。对于启动子的子区域生成了荧光素酶报告基因构建体，该子区域包含具有基本螺旋-环-螺旋（bHLH）基序的转录因子的0、1、2或3个假定的结合位点。通过将小眼症重新引入缺乏表达的黑素瘤细胞中，研究了bHLH转录因子小眼症转录因子（MITF）对启动子活性的潜在贡献。生成了双向报告基因构建体，以研究gp100和CDK2转录的潜在共调控。在存在和不存在佛波醇酯十四烷酰佛波醇13-乙酸酯（TPA）的情况下评估启动子活性。 FACS分析和免疫组织学用于评估蛋白水平上gp100和CDK2表达的共同调节。发现全长启动子，包括与MITF的共有结合位点，包含抑制gp100表达的序列。 MITF引入非表达的1123黑色素瘤细胞不能恢复gp100表达水平。 TPA对任一基因的表达调控不同，这证明了免疫染色提示的gp100和CDK2缺乏共调节。当前的研究提供了对PMel17和CDK2基因转录调控的见解，这对于确定黑色素瘤细胞调节gp100和CDK2蛋白表达的策略很重要。

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