Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality

Kiyoshi Takeda1, Koichi Noguchi1, Wei Shi1, Takashi Tanaka1, Makoto Matsumoto1, Nobuaki Yoshida1, Tadamitsu Kishimoto1, Shizuo Akira1
1Departments of Biochemistry and Anatomy and Neuroscience, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663, Japan; Department of Medicine III, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565, Japan; and Research Institute, Osaka Medical Center of Maternal and Child Health, 840 Murodo-cho, Izumi, Osaka 590-02, Japan

Tóm tắt

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.

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