{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T12:42:16Z","timestamp":1788871336878,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2015,3,8]],"date-time":"2015-03-08T00:00:00Z","timestamp":1425772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"SFB","award":["518"],"award-info":[{"award-number":["518"]}]},{"name":"GRK","award":["1041"],"award-info":[{"award-number":["1041"]}]},{"name":"DFG","award":["SFB1074\/A3"],"award-info":[{"award-number":["SFB1074\/A3"]}]},{"name":"BMBF"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Hypersecretion is the major symptom of functional neuroendocrine tumours. The mechanisms that contribute to this excessive secretion of hormones are still elusive. A key event in secretion is the exit of secretory products from the Golgi apparatus.\n                    <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\n                    \u2010ribosylation factor (Arf)\n                    <jats:styled-content style=\"fixed-case\">GTP<\/jats:styled-content>\n                    ases are known to control vesicle budding and trafficking, and have a leading function in the regulation of formation of secretory granula at the Golgi. Here, we show that Arf1 is the predominant Arf protein family member expressed in the neuroendocrine pancreatic tumour cell lines\n                    <jats:styled-content style=\"fixed-case\">BON<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">QGP<\/jats:styled-content>\n                    \u20101. In\n                    <jats:styled-content style=\"fixed-case\">BON<\/jats:styled-content>\n                    cells Arf1 colocalizes with Golgi markers as well as chromogranin A, and shows significant basal activity. The inhibition of Arf1 activity or expression significantly impaired secretion of chromogranin A. Furthermore, we show that the insulin\u2010like growth factor 1 (\n                    <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                    \u20101), a major regulator of growth and secretion in\n                    <jats:styled-content style=\"fixed-case\">BON<\/jats:styled-content>\n                    cells, induces Arf1 activity. We found that activation of Arf1 upon\n                    <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                    \u20101 receptor stimulation is mediated by\n                    <jats:styled-content style=\"fixed-case\">MEK<\/jats:styled-content>\n                    \/\n                    <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>\n                    signalling pathway in\n                    <jats:styled-content style=\"fixed-case\">BON<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">QGP<\/jats:styled-content>\n                    \u20101 cells. Moreover, the activity of Arf1 in\n                    <jats:styled-content style=\"fixed-case\">BON<\/jats:styled-content>\n                    cells is mediated by autocrinely secreted\n                    <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                    \u20101, and concomitantly, autocrine\n                    <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n                    1 secretion is maintained by Arf1 activity. In summary, our data indicate an important regulatory role for Arf1 at the Golgi in hypersecretion in neuroendocrine cancer cells.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.12473","type":"journal-article","created":{"date-parts":[[2015,3,8]],"date-time":"2015-03-08T00:35:12Z","timestamp":1425774912000},"page":"948-959","source":"Crossref","is-referenced-by-count":10,"title":["<scp>IGF<\/scp>\n                    \u20101 drives chromogranin A secretion\n                    <i>via<\/i>\n                    activation of Arf1 in human neuroendocrine tumour cells"],"prefix":"10.1111","volume":"19","author":[{"given":"Christin","family":"M\u00fcnzberg","sequence":"first","affiliation":[{"name":"Department of Internal Medicine I University of Ulm Ulm Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katharina","family":"H\u00f6hn","sequence":"additional","affiliation":[{"name":"Central Facility for Electron Microscopy University of Ulm Ulm 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