کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2068840 | 1078356 | 2011 | 11 صفحه PDF | دانلود رایگان |
We have previously demonstrated that excessive mitochondrial reactive oxygen species caused by mutations in the SDHC subunit of Complex II resulted in premature death in C. elegans and Drosophila, tumors in mouse cells and infertility in transgenic mice. We now report the generation and initial characterization of conditional transgenic mice (Tet-mev-1) using our uniquely developed Tet-On/Off system, which equilibrates transgene expression to endogenous levels. The mice experienced mitochondrial respiratory chain dysfunction that induced reactive oxygen species overproduction. The mitochondrial oxidative stress resulted in excessive apoptosis leading to low birth weight and growth retardation in the neonatal developmental phase in Tet-mev-1 mice.
Journal: Mitochondrion - Volume 11, Issue 1, January 2011, Pages 155–165