Geft is dispensable for the development of the second heart field
Geft is dispensable for the development of the second heart field
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第二心脏领域的发展，Geft缺一不可
DOI：
10.5483/bmbrep.2012.45.3.153
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发表时间：
2012-03-31
期刊：
影响因子：
3.8
通讯作者：
Wu, Xiushan
中科院分区：
文献类型：
--
作者：
Fan, Xiongwei;Hou, Ning;Wu, Xiushan
Geft是一种鸟嘌呤核苷酸交换因子，它可以通过催化结合的GDP交换GTP特异性激活小GTPase的Rho家族。Geft在心脏和骨骼肌等可兴奋组织中高度表达，在细胞增殖、迁移和细胞命运决定等许多细胞过程中起重要作用。然而，Geft在体内的作用仍然未知。在这里，我们通过将Geft的5-17外显子与loxP位点连接在一起，产生了Geft条件敲除小鼠。cre介导的Mef2c-Cre转基因小鼠心脏中Geft基因的缺失导致Geft表达的急剧下降。Geft基因敲除小鼠发育正常，无明显表型，提示Geft基因在小鼠第二心脏区发育中是不可缺少的。Geft条件敲除小鼠将成为揭示Geft在体内发育和成人体内平衡中的作用的有价值的遗传工具。（BMB报告2012；45(3):153-158）
Geft is a guanine nucleotide exchange factor, which can specifically activate Rho family of small GTPase by catalyzing the exchange of bound GDP for GTP. Geft is highly expressed in the excitable tissue as heart and skeletal muscle and plays important roles in many cellular processes, such as cell proliferation, migration, and cell fate decision. However, the in vivo role of Geft remains unknown. Here, we generated a Geft conditional knockout mouse by flanking exons 5-17 of Geft with loxP sites. Cre-mediated deletion of the Geft gene in heart using Mef2c-Cre transgenic mice resulted in a dramatic decrease of Geft expression. Geft knockout mice develop normally and exhibit no discemable phenotype, suggesting Geft is dispensable for the development of the second heart field in mouse. The Geft conditional knockout mouse will be a valuable genetic tool for uncovering the in vivo roles of Geft during development and in adult homeostasis. (BMB reports 2012; 45(3): 153-158)