Wall S R, van den Hove M F, Crepin K M, Hue L, Rousseau G G
Hormone and Metabolic Research Unit, International Institute of Cellular and Molecular Pathology, Brussels, Belgium.
FEBS Lett. 1989 Nov 6;257(2):211-4. doi: 10.1016/0014-5793(89)81536-4.
The activity of liver 6-phosphofructo-2-kinase (PFK-2), the enzyme that catalyses the synthesis of fructose 2,6-bisphosphate, was markedly decreased in hypothyroid rats and partially restored after 3 days of treatment with triiodothyronine. The changes in PFK-2 activity were accompanied by parallel changes in enzyme content measured by immunotitration and in PFK-2 mRNA determined by dot blot and Northern blot hybridization with cDNA probes. It is concluded that thyroid hormone stimulates liver PFK-2 gene expression by a pre-translational mechanism.
肝脏6-磷酸果糖-2-激酶（PFK-2）是催化果糖2,6-二磷酸合成的酶，其活性在甲状腺功能减退的大鼠中显著降低，在用三碘甲状腺原氨酸治疗3天后部分恢复。PFK-2活性的变化伴随着通过免疫滴定法测定的酶含量以及通过斑点印迹和与cDNA探针的Northern印迹杂交法测定的PFK-2 mRNA的平行变化。结论是甲状腺激素通过翻译前机制刺激肝脏PFK-2基因表达。
