Kohn A D, Chan J, Grieco D, Nikodem V M, Aloj S M, Kohn L D
Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, Maryland 20892.
Mol Endocrinol. 1989 Mar;3(3):532-8. doi: 10.1210/mend-3-3-532.
The addition of TSH to FRTL-5 thyroid cells induces a 7- to 8-fold increase in the steady state level of malic enzyme [L-malate-NADP+ oxidoreductase (decarboxylating); EC 1.1.1.40] mRNA, but does not alter beta-actin mRNA levels. Insulin alone or together with TSH has no effect on malic enzyme mRNA. The effect of TSH is not the result of thyroid hormone formation, since the addition of T3 in the presence or in the absence of TSH and the addition of 5% serum (which includes T3 and T4) have no effect. Forskolin (10(-6) M) reproduces the TSH effect, suggesting that cAMP is involved.
向FRTL - 5甲状腺细胞中添加促甲状腺激素（TSH）可使苹果酸酶[L - 苹果酸 - NADP⁺氧化还原酶（脱羧）；EC 1.1.1.40] mRNA的稳态水平增加7至8倍，但不会改变β - 肌动蛋白mRNA的水平。单独使用胰岛素或胰岛素与TSH共同作用对苹果酸酶mRNA均无影响。TSH的作用并非甲状腺激素形成的结果，因为在有或无TSH的情况下添加三碘甲状腺原氨酸（T3）以及添加5%血清（其中包含T3和甲状腺素（T4））均无作用。福斯高林（10⁻⁶ M）可重现TSH的作用，提示环磷酸腺苷（cAMP）参与其中。
