17β-estradiol upregulates distinct maxi-K channel transcripts in mouse uterus
17β-estradiol upregulates distinct maxi-K channel transcripts in mouse uterus
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DOI：
10.1016/s0303-7207(02)00136-3
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发表时间：
2002-06-28
影响因子：
4.1
通讯作者：
England, SK
中科院分区：
文献类型：
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作者：
Holdiman, AJ;Fergus, DJ;England, SK
小鼠maxi-K通道转录物经历选择性剪接以产生对细胞内调节剂的敏感性不同的同种型。我们假设17 β-雌二醇可以诱导子宫肌层maxi-K通道转录差异剪接。聚合酶链反应显示，在注射8.5 μ g 17 β-雌二醇4天或溶剂对照的小鼠中，D位点有两种产物。已知位点D的剪接调节maxi-K通道对钙和电压的敏感性。RNA酶保护分析显示，在17 β-雌二醇刺激后，a亚基转录本和编码59个氨基酸的外显子在D位点增强Ca 2+和电压敏感性，上调约1.4倍，然而，该转录本的无插入异构体增强约5倍。免疫印迹表明，总的maxi-K通道a亚基表达模拟转录调控。这些研究结果证实，maxi-K通道转录差异剪接的17 β-雌二醇，这可能有助于化学计量的变化，异构体表达在怀孕期间。(C)2002爱思唯尔科学爱尔兰有限公司保留所有权利。
The mouse maxi-K channel transcript undergoes alternative splicing to produce isoforms differing in sensitivity to intracellular regulators. We hypothesized that 17beta-estradiol could induce myometrial maxi-K channel transcripts to differentially splice. Polymerase chain reaction demonstrated two products at site D in mice injected with either 8.5 mug of 17beta-estradiol for 4 days or a vehicle control. Splicing of site D is known to modulate the sensitivity of the maxi-K channel to calcium and voltage. RNase protection analyses revealed that the a subunit transcript, and an exon encoding 59 amino acids at site D that enhances Ca2+- and voltage-sensitivity, are upregulated similar to1.4-fold after 17beta-estradiol stimulation however, the insertless isoform, of this transcript is enhanced similar to5-fold. Immunoblotting demonstrates that the total maxi-K channel a subunit expression mimics transcript regulation. These findings verify that maxi-K channel transcripts are differentially spliced by 17beta-estradiol, which may contribute to stoichiometric changes in isoform expression during pregnancy. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.