{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T23:48:50Z","timestamp":1789516130394,"version":"build-2803163510"},"reference-count":0,"publisher":"National Academy of Sciences","issue":"15","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1991,8]]},"abstract":"<jats:p>omega-Aga-IIIA, an 8.5-kDa peptide toxin isolated from the venom of Agelenopsis aperta, was found to be a highly potent inhibitor of Ca channels in cardiac muscle and in peripheral and central neurons of rats and frogs. Cardiac L-type Ca channels were completely (Kd approximately 0.6 nM) blocked by omega-Aga-IIIA. In sensory neurons, the toxin inhibited most high-threshold Ca current but not T-type Ca current. omega-Aga-IIIA blocked with similar potency (Kd approximately 1.5 nM) both omega-conotoxin GVIA-sensitive and dihydropyridine-sensitive current components but left a fraction (approximately 35%) of high-threshold current that was also resistant to omega-conotoxin and dihydropyridines. The toxin blocks N- and L-type channels with equal potency and therefore may identify a high-affinity binding site common to these two Ca channel types.<\/jats:p>","DOI":"10.1073\/pnas.88.15.6628","type":"journal-article","created":{"date-parts":[[2006,5,31]],"date-time":"2006-05-31T07:43:42Z","timestamp":1149061422000},"page":"6628-6631","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":69,"title":["Inhibition of N- and L-type Ca2+ channels by the spider venom toxin omega-Aga-IIIA."],"prefix":"10.1073","volume":"88","author":[{"given":"I M","family":"Mintz","sequence":"first","affiliation":[{"name":"Department of Neurobiology, Harvard Medical School, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V J","family":"Venema","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Harvard Medical School, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M E","family":"Adams","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Harvard Medical School, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B P","family":"Bean","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Harvard Medical School, Boston, MA 02115."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1991,8]]},"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.88.15.6628","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,13]],"date-time":"2022-04-13T13:08:26Z","timestamp":1649855306000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/full\/10.1073\/pnas.88.15.6628"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1991,8]]},"references-count":0,"journal-issue":{"issue":"15","published-print":{"date-parts":[[1991,8]]}},"alternative-id":["10.1073\/pnas.88.15.6628"],"URL":"https:\/\/doi.org\/10.1073\/pnas.88.15.6628","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[1991,8]]},"assertion":[{"value":"1991-08-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}