Abstract
The mouse maxi-K channel transcript undergoes alternative splicing to produce isoforms differing in sensitivity to intracellular regulators. We hypothesized that 17β-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 μg of 17β-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 α subunit transcript, and an exon encoding 59 amino acids at site D that enhances Ca2+- and voltage-sensitivity, are upregulated ∼1.4-fold after 17β-estradiol stimulation however, the insertless isoform of this transcript is enhanced ∼5-fold. Immunoblotting demonstrates that the total maxi-K channel α subunit expression mimics transcript regulation. These findings verify that maxi-K channel transcripts are differentially spliced by 17β-estradiol, which may contribute to stoichiometric changes in isoform expression during pregnancy.
Original language | English |
---|---|
Pages (from-to) | 1-6 |
Number of pages | 6 |
Journal | Molecular and Cellular Endocrinology |
Volume | 192 |
Issue number | 1-2 |
DOIs | |
State | Published - Jun 28 2002 |
Keywords
- Estrogen
- Maxi-K channel
- Mouse
- Splicing
- Uterus