| First Author | Holdiman AJ | Year | 2002 |
| Journal | Mol Cell Endocrinol | Volume | 192 |
| Issue | 1-2 | Pages | 1-6 |
| PubMed ID | 12088861 | Mgi Jnum | J:78060 |
| Mgi Id | MGI:2183249 | Doi | 10.1016/s0303-7207(02)00136-3 |
| Citation | Holdiman AJ, et al. (2002) 17beta-Estradiol upregulates distinct maxi-K channel transcripts in mouse uterus. Mol Cell Endocrinol 192(1-2):1-6 |
| abstractText | 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 microg 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 alpha subunit transcript, and an exon encoding 59 amino acids at site D that enhances Ca(2+)- and voltage-sensitivity, are upregulated approximately 1.4-fold after 17beta-estradiol stimulation however, the insertless isoform of this transcript is enhanced approximately 5-fold. Immunoblotting demonstrates that the total maxi-K channel alpha 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. |
