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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Millar J A, Cumming R L, Smith J A, Goldberg A

Biochem J. 1970 Oct;119(4):643-9. doi: 10.1042/bj1190643.

The mechanism of the stimulation of ferritin synthesis by iron in vivo has been studied in rat liver. Ferritin synthesis and turnover was measured by [(14)C]leucine incorporation. 2. Actinomycin D had no inhibitory effect, after administration of iron, on [(14)C]leucine incorporation into ferritin but appeared to augment the effect of iron on ferritin synthesis. 3. Cycloheximide completely abolished the stimulation by iron of [(14)C]leucine into ferritin and was subsequently utilized to show that iron acts in vivo by translational induction of apoferritin synthesis, rather than by stabilization of apoferritin or its precursors. 4. This conclusion was confirmed by showing that 2 days after acute bleeding, when iron was in the process of being removed from hepatic ferritin stores, ferritin synthesis was decreased whereas breakdown rates were unchanged.

已在大鼠肝脏中研究了体内铁刺激铁蛋白合成的机制。通过[¹⁴C]亮氨酸掺入法测定铁蛋白的合成和周转。2. 给予铁后，放线菌素D对[¹⁴C]亮氨酸掺入铁蛋白没有抑制作用，反而似乎增强了铁对铁蛋白合成的影响。3. 环己酰亚胺完全消除了铁对[¹⁴C]亮氨酸掺入铁蛋白的刺激作用，随后被用于表明铁在体内通过脱铁铁蛋白合成的翻译诱导起作用，而不是通过稳定脱铁铁蛋白或其前体起作用。4. 急性出血2天后，当铁正从肝脏铁蛋白储存中被清除时，铁蛋白合成减少而分解速率不变，这一结果证实了该结论。

Millar J A, Cumming R L, Smith J A, Goldberg A

Biochem J. 1970 Oct;119(4):643-9. doi: 10.1042/bj1190643.

The mechanism of the stimulation of ferritin synthesis by iron in vivo has been studied in rat liver. Ferritin synthesis and turnover was measured by [(14)C]leucine incorporation. 2. Actinomycin D had no inhibitory effect, after administration of iron, on [(14)C]leucine incorporation into ferritin but appeared to augment the effect of iron on ferritin synthesis. 3. Cycloheximide completely abolished the stimulation by iron of [(14)C]leucine into ferritin and was subsequently utilized to show that iron acts in vivo by translational induction of apoferritin synthesis, rather than by stabilization of apoferritin or its precursors. 4. This conclusion was confirmed by showing that 2 days after acute bleeding, when iron was in the process of being removed from hepatic ferritin stores, ferritin synthesis was decreased whereas breakdown rates were unchanged.

已在大鼠肝脏中研究了体内铁刺激铁蛋白合成的机制。通过[¹⁴C]亮氨酸掺入法测定铁蛋白的合成和周转。2. 给予铁后，放线菌素D对[¹⁴C]亮氨酸掺入铁蛋白没有抑制作用，反而似乎增强了铁对铁蛋白合成的影响。3. 环己酰亚胺完全消除了铁对[¹⁴C]亮氨酸掺入铁蛋白的刺激作用，随后被用于表明铁在体内通过脱铁铁蛋白合成的翻译诱导起作用，而不是通过稳定脱铁铁蛋白或其前体起作用。4. 急性出血2天后，当铁正从肝脏铁蛋白储存中被清除时，铁蛋白合成减少而分解速率不变，这一结果证实了该结论。