甲状腺功能亢进对转基因小鼠中磷酸烯醇式丙酮酸羧激酶/牛生长激素基因表达的影响。
Effects of hyperthyroidism on expression of a phosphoenolpyruvate carboxykinase/bovine growth hormone gene in transgenic mice.
作者信息
Xu C, McGrane M M
机构信息
Department of Nutritional Sciences, University of Connecticut, Storrs 06269, USA.
出版信息
Biochem Biophys Res Commun. 1996 Jan 17;218(2):473-9. doi: 10.1006/bbrc.1996.0084.
Thyroid hormone (T3) responsiveness of the PEPCK promoter in vivo was examined in both PEPCK/bGH(460) and PEPCK/bGH(335) mouse lines. Transgenic and non-transgenic littermates were treated with methimazole or PTU for 6 or 4 weeks, respectively, then treated +/- T3 for 10 days. In PEPCK/bGH(460) and PEPCK/bGH(355) transgenic mice, the bGH mRNA was decreased by 65% and 46%, respectively, in hyperthyroid mice when compared to euthyroid controls. Endogenous PEPCK mRNA was decreased by 33% in hyperthyroid non-transgenic mice. The conclusion of this study is that chronic hyperthyroidism in mice inhibits PEPCK-directed expression of the transgene when either the -460/+73 or the -355/+73 promoter/regulatory elements are used.
在PEPCK/bGH(460)和PEPCK/bGH(335)小鼠品系中检测了磷酸烯醇式丙酮酸羧激酶（PEPCK）启动子在体内对甲状腺激素（T3）的反应性。分别用甲巯咪唑或丙硫氧嘧啶处理转基因和非转基因同窝小鼠6周或4周，然后用±T3处理10天。与甲状腺功能正常的对照相比，在PEPCK/bGH(460)和PEPCK/bGH(355)转基因小鼠中，甲状腺功能亢进小鼠的bGH mRNA分别降低了65%和46%。甲状腺功能亢进的非转基因小鼠中内源性PEPCK mRNA降低了33%。本研究的结论是，当使用-460/+73或-355/+73启动子/调控元件时，小鼠的慢性甲状腺功能亢进会抑制转基因的PEPCK定向表达。
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