α1-蛋白酶抑制剂基因在小鼠和人类中的差异表达。
Divergent expression of alpha1-protease inhibitor genes in mouse and human.
作者信息
Tardiff J, Krauter K S
机构信息
Department of Molecular, Cellular and Developmental Biology, University of Colorado at Boulder, Campus Box 347, Boulder, CO 80309, USA.
出版信息
Nucleic Acids Res. 1998 Aug 15;26(16):3794-9. doi: 10.1093/nar/26.16.3794.
The alpha1-protease inhibitor proteins of laboratory mice are homologous in sequence and function to human alpha1-antitrypsin and are encoded by a highly conserved multigene family comprised of five members. In humans, the inhibitor is expressed in liver and in macrophages and decreased expression or inhibitory activity is associated with a deficiency syndrome which can result in emphysema and liver disease in affected individuals. It has been proposed that macrophage expression may be an important component of the function of human alpha1-antitrypsin. Clearly, it is desirable to develop a mouse model of this deficiency syndrome, however, efforts to do this have been largely unsuccessful. In this paper, we report that aside from the issues of potentially redundant gene function, the mouse may not be a suitable animal for such studies, because there is no significant expression of murine alpha1-protease inhibitor in the macrophages of mice. This difference between the species appears to result from an absence of a functional macrophage-specific promoter in mice.
实验室小鼠的α1-蛋白酶抑制剂蛋白在序列和功能上与人类α1-抗胰蛋白酶同源，由一个由五个成员组成的高度保守的多基因家族编码。在人类中，该抑制剂在肝脏和巨噬细胞中表达，表达降低或抑制活性与一种缺陷综合征相关，这种综合征可导致受影响个体患肺气肿和肝病。有人提出，巨噬细胞表达可能是人类α1-抗胰蛋白酶功能的一个重要组成部分。显然，开发这种缺陷综合征的小鼠模型是很有必要的，然而，为此所做的努力大多没有成功。在本文中，我们报告说，除了潜在的基因功能冗余问题外，小鼠可能不是进行此类研究的合适动物，因为小鼠巨噬细胞中没有显著的鼠α1-蛋白酶抑制剂表达。物种之间的这种差异似乎是由于小鼠缺乏功能性巨噬细胞特异性启动子所致。
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