Generation and characterization of mice with a conditional null allele of the HtrA4 gene.
Generation and characterization of mice with a conditional null allele of the HtrA4 gene.
复制标题
具有 HtrA4 基因条件无效等位基因的小鼠的生成和表征。
DOI：
10.3892/mmr.2015.4291
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发表时间：
2015-11
影响因子：
3.4
通讯作者：
Hoh J
中科院分区：
文献类型：
--
作者：
Liu J;Li Y;Hoh J
高温需要因子A4 （HtrA4）是丝氨酸肽酶HtrA家族的一员，参与调节蛋白质-蛋白质相互作用。关于HtrA4在人类和小鼠模型中的功能知之甚少。为了深入了解HtrA4在体内的作用，通过将HtrA4的第4、5和6外显子与loxP位点连接在一起，产生了具有条件空等位基因的小鼠。cre介导的重组，使用一个普遍活跃的Rosa26-Cre系，导致小鼠基因组中絮凝区域的缺失。重组等位基因（HtrA4−/−）纯合的小鼠存活、可育且表现正常。在冠状血管和胎盘中检测到HtrA4蛋白。然而，HtrA4的缺失并不影响心脏和胎盘的基本功能。这些小鼠具有HtrA4的条件空等位基因，可能为研究HtrA4在冠心病和子痫前期的发展和发病机制中的作用提供了有价值的工具。
High temperature requirement factor A4 (HtrA4) is a member of the HtrA family of serine peptidases involved in regulating protein-protein interactions. Little is known regarding the function of HtrA4 in humans and in mouse models. To gain insights into the role of HtrA4 in vivo, mice were generated with a conditional null allele of HtrA4 by flanking exons 4, 5 and 6 with loxP sites. Cre-mediated recombination, using a ubiquitously active Rosa26-Cre line, resulted in the deletion of the floxed region in the mouse genome. Mice homozygous for the recombinant allele (HtrA4−/−) were viable, fertile and appeared to be normal. The HtrA4 protein was detectable in coronary vessels and in the placenta. However, the loss of HtrA4 affected neither the basic heart nor placental functions. These mice, featuring a conditional null allele of HtrA4, may provide a valuable tool to investigate the role of HtrA4 in development and pathogenesis of coronary heart disease and preeclampsia.