{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T16:06:35Z","timestamp":1787241995258,"version":"build-2736575974"},"reference-count":36,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2001,3,1]]},"abstract":"<jats:p>\n                    In the cholecystokinin (CCK) hyperstimulation model of acute pancreatitis, two early intracellular events, activation of trypsinogen and activation of nuclear factor-\u03baB (NF-\u03baB), are thought to be important in the development of the disease. In this study, the relationship between these two events was investigated. NF-\u03baB activity was monitored by using a DNA binding assay and mob-1 chemokine gene expression. Intracellular trypsin activity was measured by using a fluorogenic substrate. Protease inhibitors including FUT-175, Pefabloc, and E-64d prevented CCK stimulation of intracellular trypsinogen and NF-\u03baB activation. Likewise, the NF-\u03baB inhibitors pyrrolidine dithiocarbamate and N-acetyl-l-cysteine inhibited CCK stimulation of NF-\u03baB and intracellular trypsinogen activation. These results suggested a possible codependency of these two events. However, CCK stimulated NF-\u03baB activation in Chinese hamster ovary-CCK\n                    <jats:sub>A<\/jats:sub>\n                    cells, which do not express trypsinogen, indicating that trypsin is not necessary for CCK activation of NF-\u03baB. Furthermore, adenovirus-mediated expression in acinar cells of active p65 subunits to stimulate NF-\u03baB, or of inhibitory \u03baB-\u03b1 molecules to inhibit NF-\u03baB, did not affect either basal or CCK-mediated trypsinogen activation. Thus trypsinogen and NF-\u03baB activation are independent events stimulated by CCK.\n                  <\/jats:p>","DOI":"10.1152\/ajpcell.2001.280.3.c465","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T15:24:39Z","timestamp":1514129079000},"page":"C465-C472","source":"Crossref","is-referenced-by-count":63,"title":["CCK independently activates intracellular trypsinogen and NF-\u03baB in rat pancreatic acinar cells"],"prefix":"10.1152","volume":"280","author":[{"given":"Bing","family":"Han","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0622"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baoan","family":"Ji","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0622"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig 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