17β-estradiol upregulates distinct maxi-K channel transcripts in mouse uterus

被引:26
作者
Holdiman, AJ [1 ]
Fergus, DJ [1 ]
England, SK [1 ]
机构
[1] Univ Iowa, Dept Physiol & Biophys, Iowa City, IA 52242 USA
关键词
mouse; uterus; estrogen; splicing; maxi-K channel;
D O I
10.1016/S0303-7207(02)00136-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:1 / 6
页数:6
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