SILENCING THE TYPE-II SODIUM-CHANNEL GENE - A MODEL FOR NEURAL-SPECIFIC GENE-REGULATION
SILENCING THE TYPE-II SODIUM-CHANNEL GENE - A MODEL FOR NEURAL-SPECIFIC GENE-REGULATION
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DOI：
10.1016/0896-6273(92)90218-3
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发表时间：
1992-07-01
期刊：
影响因子：
16.2
通讯作者：
MANDEL, G
中科院分区：
文献类型：
--
作者：
KRANER, SD;CHONG, JA;MANDEL, G
钠通道迷你基因的神经特异性表达已被证明是由一个28 bp的沉默元件RE1介导的，该元件位于该基因的5'侧区。该元素仅在不表达内源性脑II型钠通道基因的细胞系中有活性，包括成纤维细胞、骨骼肌和某些神经细胞系。所有这些非II型表达细胞都含有re1结合复合物。基于突变分析和体内“阻遏物陷阱”实验，我们提出细胞特异性re1结合蛋白至少在一定程度上限制了II型钠通道基因在脊椎动物神经系统中特定神经元的表达。
Neural-specific expression of a sodium channel mini-gene has been shown to be mediated by a 28 bp silencer element, RE1, located in the 5' flanking region of the gene. This element is active exclusively in cell lines that do not express the endogenous brain type II sodium channel gene, including fibroblast, skeletal muscle, and certain neuronal cell lines. All of these non-type II expressing cells contain RE1-binding complexes. On the basis of mutational analysis and in vivo "repressor trap" experiments, we propose that cell-specific RE1-binding proteins are responsible, at least in part, for restricting expression of the type II sodium channel gene to specific neurons in the vertebrate nervous system.