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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

Mazurkiewicz D, Saggerson E D

Department of Biochemistry, University College London, U.K.

Biochem J. 1989 Nov 1;263(3):829-35. doi: 10.1042/bj2630829.

Synaptosomal membranes were isolated from rats made hypothyroid by treatment with propylthiouracil and a low iodine diet. 2. When assayed in the presence of 100 mM-Na+, inhibition of forskolin-stimulated adenylate cyclase by GTP was enhanced in membranes from hypothyroid animals. 3. Hypothyroidism also enhanced inhibition of adenylate cyclase by phenylisopropyladenosine (with 100 mM-Na+ and 10 microM-GTP present). 4. Hypothyroidism did not increase binding of the A1 adenosine receptor agonist phenylisopropyladenosine to synaptosomal membranes; rather, the maximum binding was slightly decreased without any change in the KD. 5. The effect of GTP in modifying the displacement of the antagonist [3H]diethylphenylxanthine from synaptosomal membranes by unlabelled phenylisopropyladenosine was more pronounced in the hypothyroid state. 6. These findings are consistent with hypothyroidism causing modification of the brain adenylate cyclase system at the level of the coupling protein Gi.

从用丙硫氧嘧啶和低碘饮食处理而导致甲状腺功能减退的大鼠中分离出突触体膜。2. 当在100 mM - Na⁺存在的情况下进行测定时，甲状腺功能减退动物的膜中，GTP对福斯高林刺激的腺苷酸环化酶的抑制作用增强。3. 甲状腺功能减退还增强了苯异丙腺苷对腺苷酸环化酶的抑制作用（存在100 mM - Na⁺和10 μM - GTP）。4. 甲状腺功能减退并未增加A1腺苷受体激动剂苯异丙腺苷与突触体膜的结合；相反，最大结合略有下降，而解离常数（KD）没有任何变化。5. 在甲状腺功能减退状态下，GTP对未标记的苯异丙腺苷从突触体膜置换拮抗剂[³H]二乙苯基黄嘌呤的影响更为明显。6. 这些发现与甲状腺功能减退在偶联蛋白Gi水平上导致脑腺苷酸环化酶系统改变是一致的。

Mazurkiewicz D, Saggerson E D

Department of Biochemistry, University College London, U.K.

Biochem J. 1989 Nov 1;263(3):829-35. doi: 10.1042/bj2630829.

Synaptosomal membranes were isolated from rats made hypothyroid by treatment with propylthiouracil and a low iodine diet. 2. When assayed in the presence of 100 mM-Na+, inhibition of forskolin-stimulated adenylate cyclase by GTP was enhanced in membranes from hypothyroid animals. 3. Hypothyroidism also enhanced inhibition of adenylate cyclase by phenylisopropyladenosine (with 100 mM-Na+ and 10 microM-GTP present). 4. Hypothyroidism did not increase binding of the A1 adenosine receptor agonist phenylisopropyladenosine to synaptosomal membranes; rather, the maximum binding was slightly decreased without any change in the KD. 5. The effect of GTP in modifying the displacement of the antagonist [3H]diethylphenylxanthine from synaptosomal membranes by unlabelled phenylisopropyladenosine was more pronounced in the hypothyroid state. 6. These findings are consistent with hypothyroidism causing modification of the brain adenylate cyclase system at the level of the coupling protein Gi.

从用丙硫氧嘧啶和低碘饮食处理而导致甲状腺功能减退的大鼠中分离出突触体膜。2. 当在100 mM - Na⁺存在的情况下进行测定时，甲状腺功能减退动物的膜中，GTP对福斯高林刺激的腺苷酸环化酶的抑制作用增强。3. 甲状腺功能减退还增强了苯异丙腺苷对腺苷酸环化酶的抑制作用（存在100 mM - Na⁺和10 μM - GTP）。4. 甲状腺功能减退并未增加A1腺苷受体激动剂苯异丙腺苷与突触体膜的结合；相反，最大结合略有下降，而解离常数（KD）没有任何变化。5. 在甲状腺功能减退状态下，GTP对未标记的苯异丙腺苷从突触体膜置换拮抗剂[³H]二乙苯基黄嘌呤的影响更为明显。6. 这些发现与甲状腺功能减退在偶联蛋白Gi水平上导致脑腺苷酸环化酶系统改变是一致的。