Sugimoto K, Tsuboi A, Miyatake S, Arai K, Arai N
Department of Molecular Biology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304-1104.
Int Immunol. 1990;2(8):787-94. doi: 10.1093/intimm/2.8.787.
The upstream region of the mouse granulocyte macrophage colony stimulating factor (GM-CSF) gene between positions -95 and -73 is required for phorbol-12-myristate-13-acetate (PMA)- and calcium ionophore (A23187)-inducible transcriptional activity in vivo. To study the mechanism of GM-CSF gene activation in T cells, nuclear extracts from non-stimulated and PMA/A23187-stimulated Jurkat cells were used in DNA binding assays. DNA mobility shift assays with wild type and mutant oligonucleotides revealed that this region contains at least two DNA binding motifs. One is the binding sequence GGTAGTTCCCC (positions -91 to -81), recognized by NF-GM2 (nuclear factor of GM-CSF 2), and the other is a GC-rich sequence (GC-box). NF-GM2, induced in Jurkat cells by PMA/A23187 stimulation, effectively competed with DNA containing the NF-kappa B binding sequence, suggesting that it has NF-kappa B-like activity. By UV cross-linking analysis, three cross-linked bands, corresponding to Mr 165, 70, and 60 kd for NF-GM2, and 110 and 130 kd for A1 and A2, respectively, were identified. Transfection experiments showed that activation of the GM-CSF gene in response to PMA/A23187 stimulation was abolished by point mutations in either the GC-box or the NF-GM2 site; these mutations also abolished binding of the respective proteins. These results indicate that constitutive (GC-box binding factor) and inducible (NF-GM2) factors regulate the GM-CSF promoter co-operatively in a PMA/A23187-inducible manner in vivo.
小鼠粒细胞巨噬细胞集落刺激因子(GM-CSF)基因位于-95至-73位之间的上游区域,是佛波醇-12-肉豆蔻酸酯-13-乙酸酯(PMA)和钙离子载体(A23187)在体内诱导转录活性所必需的。为了研究T细胞中GM-CSF基因激活的机制,在DNA结合试验中使用了未刺激的和PMA/A23187刺激的Jurkat细胞的核提取物。用野生型和突变型寡核苷酸进行的DNA迁移率变动分析表明,该区域至少包含两个DNA结合基序。一个是由NF-GM2(GM-CSF 2的核因子)识别的结合序列GGTAGTTCCCC(-91至-81位),另一个是富含GC的序列(GC框)。PMA/A23187刺激在Jurkat细胞中诱导产生的NF-GM2,能有效地与含有NF-κB结合序列的DNA竞争,这表明它具有类NF-κB活性。通过紫外线交联分析,鉴定出了三条交联带,分别对应于NF-GM2的分子量为165、70和60 kd,以及A1和A2的分子量为110和130 kd。转染实验表明,GC框或NF-GM2位点的点突变消除了对PMA/A23187刺激的GM-CSF基因激活;这些突变也消除了相应蛋白质的结合。这些结果表明,组成型(GC框结合因子)和诱导型(NF-GM2)因子在体内以PMA/A23187诱导的方式协同调节GM-CSF启动子。