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首页> 外文期刊>Molecular and Cellular Biology >Cardiovascular and Craniofacial Defects in Crk-Null Mice
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Cardiovascular and Craniofacial Defects in Crk-Null Mice

机译：Crk空小鼠的心血管和颅面缺陷

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The Crk adaptor protein, which is encoded by two splice variants termed CrkI and CrkII, contains both SH2 and SH3 domains but no catalytic region. It is thought to function in signal transduction processes involved in growth regulation, cell transformation, cell migration, and cell adhesion. Although the function of Crk has been studied in considerable detail in cell culture, its biological role in vivo is still unclear, and no Crk-knockout mouse model has been available. Therefore, we generated a complete null allele of Crk in mice by using the Cre-loxP recombination approach. The majority of Crk-null mice die at late stages of embryonic development, and the remainder succumb shortly after birth. Embryos lacking both CrkI and CrkII exhibited edema, hemorrhage, and cardiac defects. Immunohistochemical examination suggested that defects in vascular smooth muscle caused dilation and rupturing of blood vessels. Problems in nasal development and cleft palate were also observed. These data indicate that Crk is involved in cardiac and craniofacial development and that it plays an essential role in maintaining vascular integrity during embryonic development.
机译：Crk衔接子蛋白由称为 CrkI 和 CrkII 的两个剪接变体编码，既包含SH2和SH3结构域，又没有催化区域。人们认为它在涉及生长调节，细胞转化，细胞迁移和细胞粘附的信号转导过程中起作用。尽管已在细胞培养中对Crk的功能进行了相当详细的研究，但其在体内的生物学作用仍不清楚，并且尚无 Crk 敲除小鼠模型。因此，我们通过使用Cre-loxP重组方法在小鼠中生成了 Crk 的完整无效等位基因。大多数 Crk -null小鼠死于胚胎发育的晚期，其余的死于出生后不久。同时缺乏CrkI和CrkII的胚胎表现出水肿，出血和心脏缺陷。免疫组织化学检查表明，血管平滑肌缺陷导致血管扩张和破裂。还观察到鼻部发育和pa裂问题。这些数据表明，Crk参与心脏和颅面的发育，并且在胚胎发育过程中对维持血管完整性起着至关重要的作用。

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