Izquierdo J M, Cuezva J M
Departamento de Biologia Molecular, Universidad Autónoma de Madrid, Spain.
FEBS Lett. 1993 May 24;323(1-2):109-12. doi: 10.1016/0014-5793(93)81459-d.
Thyroid hormones acutely regulate gene expression of the beta-catalytic subunit of the mitochondrial F1-ATPase complex in the liver of hypothyroid rat neonates at either a transcriptional and/or post-transcriptional level [(1990) J. Biol. Chem. 265, 9090-9097]. Administration at birth of various thyroid hormone doses to hypothyroid newborn rats promote a rapid (1 h) increase in liver steady-state amounts of both beta-F1-ATPase protein and mRNA. Induction of the beta-F1-ATPase mRNA is coincident with an elevation in gene transcription detected using nascent RNA chains synthesized by isolated nuclei. These results suggest that thyroid hormones induction of postnatal mitochondrial differentiation in the liver of hypothyroid rat neonates is mostly triggered by transcriptional regulation of beta-F1-ATPase gene.
甲状腺激素可在转录和/或转录后水平上,对甲状腺功能减退新生大鼠肝脏中线粒体F1 - ATP酶复合体的β催化亚基的基因表达进行急性调节[(1990年)《生物化学杂志》265卷,9090 - 9097页]。给甲状腺功能减退的新生大鼠在出生时给予不同剂量的甲状腺激素,可促使肝脏中β - F1 - ATP酶蛋白和mRNA的稳态量迅速(1小时)增加。β - F1 - ATP酶mRNA的诱导与使用分离细胞核合成的新生RNA链检测到的基因转录升高相一致。这些结果表明,甲状腺激素诱导甲状腺功能减退新生大鼠肝脏产后线粒体分化主要是由β - F1 - ATP酶基因的转录调控触发的。