Bikle D D, Morrissey R L, Zolock D T, Herman R H
J Lab Clin Med. 1979 Jul;94(1):88-94.
We observed that inhibitors of RNA synthesis, actinomycin D and cordycepin, stimulate chick duodenal alk Pase activity by means which are additive to the stimulaation by the biologically active metabolite of vitamin D3, 1,12(OH)2D3, and its analogue, 1 alpha OH D3. The protein synthesis inhibitor, cycloheximide, inhibited basal alk Pase activity and blocked its stimulation by actinomycin D and 1,25(OH)2D3. Both actinomycin D and cycloheximide blocked the ability of 1,25(OH)2D3 and 1 alpha OHD3 to raise serum calcium levels. The paradoxical stimulation of duodenal alk Pase activity by RNA synthesis inhibitors additive to the stimulation by 1,25(OH)2D3 suggests that alk Pase activity is controlled by mechanisms other than gene activation. (J LAB CLIN MED 94:88, 1979.)
我们观察到，RNA合成抑制剂放线菌素D和虫草素，通过与维生素D3的生物活性代谢物1,25(OH)2D3及其类似物1αOH D3的刺激作用相加的方式，刺激鸡十二指肠碱性磷酸酶（alk Pase）的活性。蛋白质合成抑制剂环己酰亚胺抑制了基础alk Pase活性，并阻断了放线菌素D和1,25(OH)2D3对其的刺激作用。放线菌素D和环己酰亚胺都阻断了1,25(OH)2D3和1αOH D3升高血清钙水平的能力。RNA合成抑制剂对十二指肠alk Pase活性的矛盾刺激作用与1,25(OH)2D3的刺激作用相加，这表明alk Pase活性是由基因激活以外的机制控制的。（《实验室与临床医学杂志》94:88, 1979年）
