Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality
Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality
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DOI：
10.1073/pnas.94.8.3801
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发表时间：
1997-04-15
影响因子：
11.1
通讯作者：
Akira, S
中科院分区：
文献类型：
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作者：
Takeda, K;Noguchi, K;Akira, S
信号换能器和转录激活器（STAT）蛋白已被证明可以介导对细胞因子的生物反应。Stat3是STAT家族的一员，可被多种细胞因子激活，包括白细胞介素6家族细胞因子、瘦素、粒细胞集落刺激因子和表皮生长因子。为了研究Stat3的生物学功能，我们通过基因靶向培养了Stat3缺乏的小鼠。杂合子间杂交无法获得存活的stat3缺陷小鼠。对几个妊娠期胚胎的分析显示，stat3缺陷胚胎在胚胎6.5天至7.5天之间表现出快速退化，尽管它们在胚胎6.0天之前发育到卵柱期。这些结果表明Stat3对小鼠胚胎的早期发育至关重要。
Signal transducer and activator of transcription (STAT) proteins have been shown to mediate biological actions in response to cytokines. Stat3, a member of the STAT family, is activated by a variety of cytokines, including the interleukin 6 family of cytokines, leptin, granulocyte colony-stimulating factor, and epidermal growth factor. To address the biological function of Stat3, we generated mice deficient in Stat3 by gene targeting. No viable Stat3-deficient mice could be obtained from heterozygote intercross. Analysis of embryos at several gestation times revealed that Stat3-deficient embryos showed a rapid degeneration between embryonic days 6.5 and 7.5, although they developed into the egg cylinder stage until embryonic day 6.0. These results demonstrate that Stat3 is essential for the early development of mouse embryos.