Ekker M, Doyen N, Leblond-Francillard M, Rougeon F
Unité de Génétique et Biochimie du Développement, LA CNRS 361, Institut Pasteur, Paris, France.
FEBS Lett. 1987 Oct 5;222(2):337-40. doi: 10.1016/0014-5793(87)80397-6.
A mouse renin-1 gene promoter fragment, normally inactive in B-cells, becomes a potent promoter in these cells after insertion of the highly conserved decanucleotide (dc/cd sequence) of immunoglobulin heavy and light chain promoters [(1987) EMBO J. 6, 1685-1690]. We observe retarded complexes of the same electrophoretic mobility when the cd-containing renin promoter fragment or an authentic immunoglobulin heavy chain promoter fragment is incubated with a nuclear extract from myeloma cells, suggesting that the renin promoter is activated due to its acquired ability to bind a B-cell-specific positive factor. No retarded complexes are observed with the original renin promoter fragment thus questioning the presence of a repressor as an explanation for its lack of activity in B-cells.
小鼠肾素-1基因启动子片段在B细胞中通常无活性,但在插入免疫球蛋白重链和轻链启动子的高度保守十聚体(dc/cd序列)后,在这些细胞中成为一个有效的启动子[(1987)《欧洲分子生物学组织杂志》6, 1685 - 1690]。当将含cd的肾素启动子片段或真实的免疫球蛋白重链启动子片段与骨髓瘤细胞核提取物一起孵育时,我们观察到具有相同电泳迁移率的阻滞复合物,这表明肾素启动子因获得结合B细胞特异性正性因子的能力而被激活。用原始肾素启动子片段未观察到阻滞复合物,因此对存在阻遏物作为其在B细胞中缺乏活性的解释提出质疑。