{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T16:52:32Z","timestamp":1781110352724,"version":"3.54.1"},"reference-count":52,"publisher":"National Academy of Sciences","issue":"14","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2002,7,9]]},"abstract":"<jats:p>\n                    Glucose, the principal regulator of endocrine pancreas, has several effects on pancreatic beta cells, including the regulation of insulin release, cell proliferation, apoptosis, differentiation, and gene expression. Although the sequence of events linking glycemia with insulin release is well described, the mechanism whereby glucose regulates nuclear function is still largely unknown. Here, we have shown that an ATP-sensitive K\n                    <jats:sup>+<\/jats:sup>\n                    channel (K\n                    <jats:sub>ATP<\/jats:sub>\n                    ) with similar properties to that found on the plasma membrane is also present on the nuclear envelope of pancreatic beta cells. In isolated nuclei, blockade of the K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel with tolbutamide or diadenosine polyphosphates triggers nuclear Ca\n                    <jats:sup>2+<\/jats:sup>\n                    transients and induces phosphorylation of the transcription factor cAMP response element binding protein. In whole cells, fluorescence\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization revealed that these Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals may trigger c-\n                    <jats:italic>myc<\/jats:italic>\n                    expression. These results demonstrate a functional K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel in nuclei linking glucose metabolism, nuclear Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals, and nuclear function.\n                  <\/jats:p>","DOI":"10.1073\/pnas.142039299","type":"journal-article","created":{"date-parts":[[2002,7,28]],"date-time":"2002-07-28T18:26:28Z","timestamp":1027880788000},"page":"9544-9549","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":75,"title":["Nuclear K\n                    <sub>ATP<\/sub>\n                    channels trigger nuclear Ca\n                    <sup>2+<\/sup>\n                    transients that modulate nuclear function"],"prefix":"10.1073","volume":"99","author":[{"given":"Ivan","family":"Quesada","sequence":"first","affiliation":[{"name":"Institute of Bioengineering, Miguel Hern\u00e1ndez University, San Juan Campus, 03550 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