Biggs J R, Zhang Y, Murphy E V
Department of Neurological Surgery, School of Medicine, University of California, San Francisco 94143, USA.
J Cell Physiol. 1995 Aug;164(2):249-58. doi: 10.1002/jcp.1041640205.
The Id2 gene is one of several "Id-like" genes which encode helix-loop-helix proteins which dimerize with basic helix-loop-helix proteins and inhibit binding to the DNA enhancer element known as an E box. By repressing the DNA binding activity of basic helix-loop-helix proteins, Id proteins inhibit transcription of tissue-specific genes in myoblasts, hematopoietic precursor cells, and other types of undifferentiated cells. Serum starvation results in the disappearance of Id gene transcripts in most types of cultured cells, and often induces differentiation of these cells. In order to gain some insight into this process, we have analyzed Id2 promoter function in the glioma cell line U87Y. We have isolated 300 base pairs of Id2 promoter sequence which is sufficient to repress the activity of a reporter gene in serum-starved U87Y cells, but induces the activity of the reporter gene when the cells are stimulated with fresh serum. Two regions within this 300 base pair sequence contain repressor elements; deletion of either region results in increased promoter activity. Both repressor regions serve as binding sites for a protein present in extracts from serum-starved U87Y cells but not in serum-stimulated cells.
Id2基因是几个“类Id”基因之一，这些基因编码螺旋-环-螺旋蛋白，该蛋白与碱性螺旋-环-螺旋蛋白二聚化，并抑制与被称为E盒的DNA增强子元件的结合。通过抑制碱性螺旋-环-螺旋蛋白的DNA结合活性，Id蛋白抑制成肌细胞、造血前体细胞和其他类型未分化细胞中组织特异性基因的转录。血清饥饿导致大多数类型培养细胞中Id基因转录本消失，并常常诱导这些细胞分化。为了深入了解这一过程，我们分析了胶质瘤细胞系U87Y中Id2启动子的功能。我们分离出300个碱基对的Id2启动子序列，该序列足以在血清饥饿的U87Y细胞中抑制报告基因的活性，但在用新鲜血清刺激细胞时会诱导报告基因的活性。这300个碱基对序列中的两个区域含有阻遏元件；删除任一区域都会导致启动子活性增加。两个阻遏区域都是血清饥饿的U87Y细胞提取物中存在的一种蛋白的结合位点，而血清刺激的细胞中不存在这种蛋白。
