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"The coupling between membrane receptors and MaxiK channels has been mostly studied in smooth muscle where muscle relaxants like beta-adrenergic agents and estrogen induce MaxiK channel activation and constrictors like Acetylcholine, Thromboxane A2, and Angiotensin II result in channel inhibition."

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"These data suggest that estrogen deficiency by removing ovaries upregulates KCa1.1 channel protein in Ah-type BRNs, and subsequently increases AP repolarization and blunts neuroexcitation through estrogen membrane receptor signaling."

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"Furthermore , BK channels can be modulated by estrogens such as 17beta-Estradiol ( E2 ) , when alpha subunit is co-expressed with the beta1 subunit ( Valverde et al ., 1999 ; De Wet et al ., 2006 ; Granados et al ., 2019 ) ."