{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T14:54:23Z","timestamp":1787496863343,"version":"build-2736575974"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,6,23]],"date-time":"2004-06-23T00:00:00Z","timestamp":1087948800000},"content-version":"vor","delay-in-days":2457,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Biochemistry"],"published-print":{"date-parts":[[1997,10]]},"abstract":"<jats:p>\n                    In single platelets and in suspensions of platelets, \u03b1\u2010thrombin evokes dose\u2010dependent, transient increases in cytosolic Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration, [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>ij<\/jats:sub>\n                    , which are more prolonged than the [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]; transients evoked by other platelet agonists such as the thrombin\u2010receptor\u2010activating hexapeptide SFLLRN, thromboxane A\n                    <jats:sub>2<\/jats:sub>\n                    analog U46619, and ADP As a quantity taking into account both the magnitude and length of the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    response, we defined the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010mobilizing potency (CMP) of an agonist as the integrated rise in [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    during the time of the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signal. It was observed that: (a) the CMP increased with the agonist concentration in a saturating way, its maximal value being about four\u2010times higher with \u03b1\u2010thrombin than with SFLLRN; (b) the high CMP of \u03b1\u2010thrombin was for only a small part due to endogenous production of ADP or thromboxane, and was mainly a consequence of prolonged influx of external Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ; (c) the CMP declined when a\u2010thrombin was inactivated during the course of the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signal; (d) CMP values increased with the agonist concentration upon sequential addition of increasing amounts of \u03b1\u2010thrombin or SFLLRN; (e) when \u03b1\u2010thrombin was gradually added to the platelets or formed by an in situ reconstituted prothrombinase system (with factor Xa, factor Va, and prothrombin), integrated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    responses were a function of the product of the \u03b1\u2010thrombin concentration and the time of its presence. However, in these cases, the final CMP values were independent of the rate of \u03b1\u2010thrombin addition or formation. We conclude that \u03b1\u2010thrombin\u2010induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals in platelets rely largely upon Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx, are not, or only slightly, subjected to homologous desensitization, and reflect the enzymatic capacity of \u03b1\u2010thrombin to cleave protease\u2010activated receptors. Thus, the high and prolonged Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signal induced by \u03b1\u2010thrombin is due to continuous receptor cleavage without desensitizing effects of previously cleaved receptors.\n                  <\/jats:p>","DOI":"10.1111\/j.1432-1033.1997.00547.x","type":"journal-article","created":{"date-parts":[[2004,6,23]],"date-time":"2004-06-23T12:11:24Z","timestamp":1087992684000},"page":"547-555","source":"Crossref","is-referenced-by-count":80,"title":["The Ca\n                    <sup>2+<\/sup>\n                    \u2010Mobilizing Potency of \u03b1\u2010Thrombin and Thrombin\u2010Receptor\u2010Activating Peptide on Human Platelets"],"prefix":"10.1111","volume":"249","author":[{"given":"Johan W. M.","family":"Heemskerk","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marion A. H.","family":"Feijge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lidewij","family":"Henneman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Rosing","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. Coenraad","family":"Hemker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2004,6,23]]},"reference":[{"key":"e_1_2_3_2_2","first-page":"477","volume-title":"Haemostasis and thrombosis","author":"Hemker H. 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W. M.","year":"1993","journal-title":"J. Biol. Chem."},{"key":"e_1_2_3_25_2","doi-asserted-by":"crossref","first-page":"195","DOI":"10.1007\/978-1-4615-2994-1_15","volume-title":"Mechanisms of platelet activation and control","author":"Bevers E. M.","year":"1993"},{"key":"e_1_2_3_26_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.57.070188.004411"},{"key":"e_1_2_3_27_2","doi-asserted-by":"crossref","first-page":"6556","DOI":"10.1016\/S0021-9258(20)65178-X","article-title":"Thrombin\u2010catalyzed activation of human coagulation factor V","volume":"257","author":"Suzuki K.","year":"1982","journal-title":"J. Biol. 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