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首页> 外文期刊>Molecular and Cellular Biology >Targeted Deletion of mek5 Causes Early Embryonic Death and Defects in the Extracellular Signal-Regulated Kinase 5/Myocyte Enhancer Factor 2 Cell Survival Pathway
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Targeted Deletion of mek5 Causes Early Embryonic Death and Defects in the Extracellular Signal-Regulated Kinase 5/Myocyte Enhancer Factor 2 Cell Survival Pathway

机译：有针对性的删除mek5导致早期胚胎死亡和细胞外信号调节激酶5 /心肌细胞增强因子2细胞存活途径中的缺陷。

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To elucidate the physiological significance of MEK5 in vivo, we have examined the effect of mek5 gene elimination in mice. Heterozygous mice appear to be healthy and were fertile. However, mek5?/? embryos die at approximately embryonic day 10.5 (E10.5). The phenotype of the mek5?/? embryos includes abnormal cardiac development as well as a marked decrease in proliferation and an increase in apoptosis in the heart, head, and dorsal regions of the mutant embryos. The absence of MEK5 does not affect cell cycle progression but sensitizes mouse embryonic fibroblasts (MEFs) to the ability of sorbitol to enhance caspase 3 activity. Further studies with mek5?/? MEFs indicate that MEK5 is required for mediating extracellular signal-regulated kinase 5 (ERK5) activation and for the regulation of the transcriptional activity of myocyte enhancer factor 2. Overall, this is the first study to rigorously establish the role of MEK5 in vivo as an activator of ERK5 and as an essential regulator of cell survival that is required for normal embryonic development.
机译：为了阐明MEK5在体内的生理意义，我们研究了 mek5 基因消除在小鼠中的作用。杂合小鼠看来是健康的，并且能够繁殖。但是， mek5 ？ / ？胚胎在大约第10.5天（E10.5）死亡。 mek5 ？ / ？胚胎的表型包括异常的心脏发育以及明显的增殖和减少。突变胚胎的心脏，头部和背部区域的凋亡增加。没有MEK5不会影响细胞周期进程，但会使小鼠胚胎成纤维细胞（MEF）对山梨糖醇增强caspase 3活性的能力敏感。对 mek5 ？ / ？ MEF的进一步研究表明，MEK5是介导细胞外信号调节激酶5（ ERK5）激活并调节肌细胞增强因子2的转录活性。总体而言，这是第一个严格确立MEK5在体内作为ERK5激活剂和细胞存活所必需的重要调节剂的作用的研究。胚胎发育正常。

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