Pan L C, Price P A
J Biol Chem. 1984 May 10;259(9):5844-7.
The stimulation of bone gamma-carboxyglutamic acid protein (BGP) synthesis by 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) in clonal osteosarcoma cell culture has been analyzed using specific inhibitors of RNA and protein synthesis. Addition of actinomycin D or alpha-amanitin simultaneously with 1,25-(OH)2D3 prevented hormonal elevation of BGP levels but did not affect basal BGP synthesis. Neither transcriptional inhibitor had any effect on BGP synthesis in cultures which had already been fully stimulated by 1,25-(OH)2D3. In contrast, the protein synthesis inhibitor cycloheximide blocked BGP synthesis in both untreated and 1,25-(OH)2D3-treated cells. Inhibitor effects on media BGP levels corresponded in all cases to effects on the rapidly turned over intracellular BGP pool. These results support a model of transcriptional control for the action of 1,25-(OH)2D3 and suggest that the hormone elicits a transient burst of transcription of the BGP gene.
利用RNA和蛋白质合成的特异性抑制剂，对克隆性骨肉瘤细胞培养中1,25 - 二羟基维生素D3（1,25-(OH)2D3）刺激骨γ-羧基谷氨酸蛋白（BGP）合成的情况进行了分析。与1,25-(OH)2D3同时添加放线菌素D或α-鹅膏蕈碱可阻止BGP水平的激素性升高，但不影响基础BGP合成。两种转录抑制剂对已被1,25-(OH)2D3充分刺激的培养物中的BGP合成均无任何影响。相比之下，蛋白质合成抑制剂环己酰亚胺在未处理和1,25-(OH)2D3处理的细胞中均阻断BGP合成。抑制剂对培养基中BGP水平的影响在所有情况下均与对快速周转的细胞内BGP池的影响相对应。这些结果支持了1,25-(OH)2D3作用的转录控制模型，并表明该激素引发了BGP基因转录的短暂爆发。
