Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Beta-endorphin and naloxone bind to Jurkat cell membrane preparations and can mutually displace each other from membrane binding sites. Tetraethylammonium ion, a potassium channel blocker, competitively displaces beta-endorphin and naloxone from membrane binding sites. Mitogen stimulated calcium ion flux is inhibited by tetraethyl ammonium and this inhibition is relieved by naloxone. With data derived from whole cell calcium ion flux studies, we accurately calculated the competitive displacement of beta-endorphin and naloxone from membrane preparations by tetraethylammonium thus showing that the action of these agents on potassium channels does not require second messengers. Using the resuspension induced ion flux technique, we find that beta-endorphin competes against naloxone for binding to Jurkat cells and naloxone competes against charybdotoxin, a potassium channel inhibitor, which like tetraethylammonium, is known to bind to the outer vestibule of the channel. Patch clamp electrophysiological studies show that beta-endorphin and naloxone exert complex actions on potassium channels in the presence or absence of mitogens. We conclude that one molecule of beta-endorphin or naloxone, but not both at the same time, bind to an area near the charybdotoxin/tetraethylammonium binding locus of Jurkat potassium channels.
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PMID:The K channel blocker, tetraethylammonium, displaces beta-endorphin and naloxone from T-cell binding sites. 930 24

The present study investigated the role of K(+) channels in the inhibitory effect of glucocorticoid on adrenocorticotropin (ACTH) release induced by corticotropin-releasing hormone (CRH) using cultured rat anterior pituitary cells. Apamin and charybdotoxin (CTX) did not have a significant effect on ACTH release induced by CRH (1 nM). Tetraethylammonium (TEA), a broad spectrum K(+) channel blocker, increased the ACTH response to CRH only at the highest concentration (10 mM). The exposure to 100 nM corticosterone for 60 min inhibited the CRH-induced ACTH release. Neither TEA, apamin, nor CTX affected the inhibitory effect of corticosterone. In contrast, astemizole (Ast) and E-4031, ether-a-go-go-related gene (erg) K(+) channel blockers, abolished the inhibitory effect of corticosterone on CRH-induced ACTH release (1.25+/-0.10 vs. 1.45+/-0.11 ng/well at 10 microM Ast, p>0.05, 1.71+/-0.16 vs. 1.91+/-0.32 ng/well at 10 microM E-4031, p>0.05, vehicle vs. corticosterone). RT-PCR demonstrated all three subtypes of rat-erg mRNAs in the pituitary and corticosterone increased only erg1 mRNA up to 2.47+/-0.54 fold. In conclusion, erg K(+) channels were up-regulated by glucocorticoid, and have indispensable roles in delayed glucocorticoid inhibition of CRH-induced ACTH release by rat pituitary cells.
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PMID:The role of ether-a-go-go-related gene K(+) channels in glucocorticoid inhibition of adrenocorticotropin release by rat pituitary cells. 1883 72