Masters B A, Kelly E J, Quaife C J, Brinster R L, Palmiter R D
Laboratory of Reproductive Physiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.
Proc Natl Acad Sci U S A. 1994 Jan 18;91(2):584-8. doi: 10.1073/pnas.91.2.584.
We inactivated the mouse metallothionein (MT)-I and MT-II genes in embryonic stem cells and generated mice homozygous for these mutant alleles. These mice were viable and reproduced normally when reared under normal laboratory conditions. They were, however, more susceptible to hepatic poisoning by cadmium. This proves that these widely expressed MTs are not essential for development but that they do protect against cadmium toxicity. These mice provide a means for testing other proposed functions of MT in vivo.
我们在胚胎干细胞中使小鼠金属硫蛋白（MT）-I和MT-II基因失活，并培育出这些突变等位基因的纯合子小鼠。在正常实验室条件下饲养时，这些小鼠能够存活并正常繁殖。然而，它们对镉引起的肝脏中毒更敏感。这证明这些广泛表达的金属硫蛋白对发育并非必不可少，但它们确实能抵御镉的毒性。这些小鼠为在体内测试金属硫蛋白的其他假定功能提供了一种手段。
