{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T03:07:35Z","timestamp":1779332855881,"version":"3.51.4"},"reference-count":20,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"5990","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2010,7,23]]},"abstract":"<jats:title>Brain Over Muscle<\/jats:title>\n          <jats:p>\n            Mutations in the gene encoding the Kir6.2 subunit of the adenosine triphosphate (ATP)\u2013sensitive potassium (K\n            <jats:sub>ATP<\/jats:sub>\n            ) channel cause a specific type of neonatal diabetes in humans, known as iDEND, which is often accompanied by muscle weakness of unknown etiology. By studying mice expressing the mutant gene only in muscle or only in nerve,\n            <jats:bold>\n              Clark\n              <jats:italic>et al.<\/jats:italic>\n            <\/jats:bold>\n            (p.\n            <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" page=\"458\" related-article-type=\"in-this-issue\" vol=\"329\" xlink:href=\"10.1126\/science.1186146\">458<\/jats:related-article>\n            , published online 1 July) found that the motor impairments originate from inappropriate activation of the channel in the central nervous system rather than in muscle. Patients with iDEND are often treated with sulphonylurea therapies that block K\n            <jats:sub>ATP<\/jats:sub>\n            channels in both brain and muscle, and these drugs can have adverse effects on heart muscle. Drugs with greater specificity for K\n            <jats:sub>ATP<\/jats:sub>\n            channels in the brain may thus be a safer option.\n          <\/jats:p>","DOI":"10.1126\/science.1186146","type":"journal-article","created":{"date-parts":[[2010,7,2]],"date-time":"2010-07-02T02:41:04Z","timestamp":1278038464000},"page":"458-461","source":"Crossref","is-referenced-by-count":92,"title":["Muscle Dysfunction Caused by a K\n            <sub>ATP<\/sub>\n            Channel Mutation in Neonatal Diabetes Is Neuronal in Origin"],"prefix":"10.1126","volume":"329","author":[{"given":"Rebecca H.","family":"Clark","sequence":"first","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James S.","family":"McTaggart","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard","family":"Webster","sequence":"additional","affiliation":[{"name":"Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roope","family":"Mannikko","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michaela","family":"Iberl","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiu Li","family":"Sim","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrik","family":"Rorsman","sequence":"additional","affiliation":[{"name":"Oxford Centre for Diabetes Endocrinology and Metabolism, Churchill Hospital, Oxford OX3 7LJ, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maike","family":"Glitsch","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Beeson","sequence":"additional","affiliation":[{"name":"Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frances M.","family":"Ashcroft","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"221","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.9.2503"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00348.2007"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature04711"},{"key":"e_1_3_2_5_2","first-page":"80","article-title":"Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetes","volume":"119","author":"Girard C. 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