首页> 美国卫生研究院文献>other >The Drosophila Midkine/Pleiotrophin Homologues Miple1 and Miple2 Affect Adult Lifespan but Are Dispensable for Alk Signaling during Embryonic Gut Formation
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The Drosophila Midkine/Pleiotrophin Homologues Miple1 and Miple2 Affect Adult Lifespan but Are Dispensable for Alk Signaling during Embryonic Gut Formation

机译:果蝇Midkine / Pleiotrophin同系物Miple1和Miple2影响成年寿命但可在胚胎肠道形成过程中传递信号给Alk。

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摘要

Midkine (MDK) and Pleiotrophin (PTN) are small heparin-binding cytokines with closely related structures. The Drosophila genome harbours two genes encoding members of the MDK/PTN family of proteins, known as miple1 and miple2. We have investigated the role of Miple proteins in vivo, in particular with regard to their proposed role as ligands for the Alk receptor tyrosine kinase (RTK). Here we show that Miple proteins are neither required to drive Alk signaling during Drosophila embryogenesis, nor are they essential for development in the fruit fly. Additionally we show that neither MDK nor PTN can activate hALK in vivo when ectopically co-expressed in the fly. In conclusion, our data suggest that Alk is not activated by MDK/PTN related growth factors Miple1 and Miple 2 in vivo.
机译:Midkine(MDK)和Pleiotrophin(PTN)是具有紧密相关结构的小肝素结合细胞因子。果蝇基因组包含两个编码MDK / PTN蛋白质家族成员的基因,称为miple1和miple2。我们已经研究了Miple蛋白在体内的作用,特别是关于它们作为Alk受体酪氨酸激酶(RTK)配体的提议作用。在这里,我们显示了在果蝇胚胎发生过程中,既不需要Miple蛋白来驱动Alk信号,也不是在果蝇中发育所必需的蛋白。此外,我们显示当异位在飞行中共表达时,MDK和PTN均不能在体内激活hALK。总之,我们的数据表明Alk在体内没有被MDK / PTN相关生长因子Miple1和Miple 2激活。

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