Comparative analysis of the human and mouse Hey1 promoter:: Hey genes are new notch target genes
Comparative analysis of the human and mouse Hey1 promoter:: Hey genes are new notch target genes
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DOI：
10.1006/bbrc.2000.3354
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发表时间：
2000-08-28
影响因子：
3.1
通讯作者：
Gessler, M
中科院分区：
文献类型：
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作者：
Maier, MM;Gessler, M
Hey 基因（Hey1、Hey2 和 HeyL）编码一组新的基本螺旋-环-螺旋转录因子，这些转录因子与分裂基因的毛/增强子相关。在本研究中，我们克隆并鉴定了人和小鼠Hey1基因的启动子区域，转录起始位点位于起始密码子上游138个核苷酸处。有一个最小序列元件（nt -30 至 -247）对于三种不同细胞类型中的基础转录至关重要。在更上游，可以鉴定出高度保守的序列块（nt -324 至 -646；类似于 90% 人/小鼠相似性），其中包含几个假定的转录因子结合位点，并且可能代表该基因的重要调控区域。共转染实验表明，所有四种哺乳动物 Notch 受体的激活形式通过两个功能性 PCBP-J kappa 结合位点上调 mHey1 启动子活性。 Hey 基因家族的其他成员 Hey2 和 HeyL，也具有 RBP-J kappa 结合位点，并且它们对 Notch 信号传导有类似的反应。因此，我们的数据清楚地表明 Hey 基因形成了一类新的 Notch 信号转导器，应该证明它与各种发育过程相关。 (C) 2000 年学术出版社。
Hey genes (Hey1, Hey2 and HeyL) encode a new group of basic helix-loop-helix transcription factors that are related to the hairy/Enhancer of split genes. In the present study, we cloned and characterized the promoter region of the human and mouse Hey1 gene, The transcription initiation site was located 138 nucleotides upstream of the start codon. There is a minimal sequence element (nt -30 to -247) that is essential and important for basal transcription in three different cell types. Further upstream, a highly conserved sequence block (nt -324 to -646; similar to 90% human/mouse similarity) could be identified that contains several putative binding sites for transcription factors and likely represents an important regulatory region for this gene, Cotransfection experiments demonstrated that the mHey1 promoter activity is up-regulated by the activated form of all four mammalian Notch receptors via two functional PCBP-J kappa binding sites, The other members of the Hey gene family, Hey2 and HeyL, also possess RBP-J kappa binding sites and they are similarily responsive to Notch signaling. Thus, our data clearly demonstrate that Hey genes form a new class of Notch signal transducers that should prove to be relevant in various developmental processes. (C) 2000 Academic Press.