Causal role for jun protein in the stimulation of choline acetyltransferase by insulin in embryonic chick retina.
Causal role for jun protein in the stimulation of choline acetyltransferase by insulin in embryonic chick retina.
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jun 蛋白在胚胎鸡视网膜中胰岛素刺激胆碱乙酰转移酶中的因果作用。
DOI：
10.1006/bbrc.1997.6374
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Hausman,RE
中科院分区：
文献类型：
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作者：
Ren,Y;Holdengreber,V;Ben-Shaul,Y;Shah,BH;Varanasi,J;Hausman,RE
先前的工作表明，在胚胎发育的关键阶段，胰岛素的可获得性刺激了乙酰胆碱合成酶-胆碱乙酰转移酶(ChAT)的活性(R.E.Hausmanet al.，1991，Dev.脑部研究报告59，31-37)。在这里，我们显示2到5分钟的胰岛素暴露会导致超过24小时的ChAT蛋白升高。在接触胰岛素后，Jun蛋白水平立即出现一过性增加，随后ChAT水平也随之增加。ChAT蛋白的刺激不是蛋白质合成的整体刺激的结果，因为其他蛋白质不受影响。将细胞暴露在Jun的反义寡核苷酸中，而不是正义寡核苷酸中，可以减少Jun和ChAT的增加。这些和以前的结果表明，胰岛素对于视网膜发育过程中ChAT蛋白的特征性增加是必要的，这种增加需要Jun的瞬时合成。
Previous work showed that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) (R. E. Hausmanet al.,1991,Dev. Brain Res.59, 31–37). Here we show that a 2- to 5-min exposure to insulin results in a greater than 24 hr elevation in ChAT protein. Immediately following exposure to insulin there is a transient increase in the level of jun protein followed by an increase in ChAT. The stimulation of ChAT protein is not the result of an overall stimulation of protein synthesis as other proteins are not affected. Exposure of the cells to antisense oligonucleotide to jun, but not to sense oligonucleotide, reduces the increase in both jun and ChAT. These and previous results suggest that insulin is necessary for the characteristic increase in ChAT protein during retina development and that this increase requires the transient synthesis of jun.