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首页> 外文期刊>Developmental cell >Casein Kinase 1 Promotes Initiation of Clathrin-Mediated Endocytosis
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Casein Kinase 1 Promotes Initiation of Clathrin-Mediated Endocytosis

机译:酪蛋白激酶1促进网格蛋白介导的内吞作用的启动。

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摘要

In budding yeast, over 60 proteins functioning in at least five modules are recruited to endocytic sites with predictable order and timing. However, how sites of clathrin-mediated endocytosis are initiated and stabilized is not well understood. Here, the casein kinase 1 (CK1) Hrr25 is shown to be an endocytic protein and to be among the earliest proteins to appear at endocytic sites. Hrr25 absence or overexpression decreases or increases the rate of endocytic site initiation, respectively. Ede1, an early endocytic Eps15-like protein important for endocytic initiation, is an Hrr25 target and is required for Hrr25 recruitment to endocytic sites. Hrr25 phosphorylation of Ede1 is required for Hrr25-Ede1 interaction and promotes efficient initiation of endocytic sites. These observations indicate that Hrr25 kinase and Ede1 cooperate to initiate and stabilize endocytic sites. Analysis of the mammalian homologs CK1 delta/epsilon suggests a conserved role for these protein kinases in endocytic site initiation and stabilization.
机译:在发芽酵母中,以可预测的顺序和时机将至少在五个模块中起作用的60多种蛋白质募集到内吞位点。但是,网格蛋白介导的内吞作用的位点如何被启动和稳定尚不清楚。在这里,酪蛋白激酶1(CK1)Hrr25被证明是一种内吞蛋白,并且是最早出现在内吞位点的蛋白之一。 Hrr25缺失或过表达分别降低或增加了内吞位点起始速率。 Ede1是一种早期内吞Eps15样蛋白,对内吞起始很重要,它是Hrr25的靶标,是Hrr25募集到内吞位点所必需的。 Hde25-Ede1相互作用需要Ede1的Hrr25磷酸化,并促进内吞位点的有效启动。这些观察结果表明Hrr25激酶和Ede1协同启动和稳定内吞位点。对哺乳动物同源物CK1δ/ε的分析表明,这些蛋白激酶在胞吞位点起始和稳定中起保守作用。

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