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XB-ART-17360
Naunyn Schmiedebergs Arch Pharmacol 1996 Dec 01;3546:698-702. doi: 10.1007/bf00166894.
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Inhibition of minK protein induced K+ channels in Xenopus oocytes by estrogens.

Waldegger S , Lang U , Herzer T , Suessbrich H , Binder K , Lepple-Wienhues A , Nagl U , Paulmichl M , Franz HB , Kiesl L , Lang F , Busch AE .


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Previously it was shown that minK protein expression in uterus is regulated by estrogen. In the present study, we were interested in putative direct effects of estrogen on minK protein induced K+ currents (IminK) in Xenopus oocytes. Superfusion with 17-beta-estradiol (1 microM) resulted in an inhibition of minK-induced currents, but had no appreciable effects on the delayed rectifier and inward rectifier K+ channels Kv1.1 and Kir2.1, respectively. The inhibition of IminK by 17-beta-estradiol was concentration-dependent, with an IC50 of approximately 0.5 microM. In the presence of 17-beta-estradiol, the conductance-voltage relationship was shifted to more depolarized potentials. IminK inhibition occurred also in the presence of the estrogen-receptor antagonist tamoxifen, suggesting that a mechanism independent of estrogen receptors is involved. The synthetic estrogen diethylstilbestrol (DES) also inhibited IminK but with a lower affinity (IC50 of 4.5 microM), while cortisol and progesterone had only weak effects on IminK. In summary, the results indicate that estrogens directly inhibit IminK.

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Species referenced: Xenopus
Genes referenced: des des.2 kcne1 mink1

References [+] :
Attali, Cloning, functional expression, and regulation of two K+ channels in human T lymphocytes. 1992, Pubmed, Xenbase