{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:21:46Z","timestamp":1792131706517,"version":"4.4.0"},"reference-count":34,"publisher":"National Academy of Sciences","issue":"1","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2014,1,7]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    Basal ganglia circuits are engaged in controlling psychomotor function. The circuits consist of striatonigral and striatopallidal pathways. The opposing but balanced activity of these two neural pathways is important for regulating movement-related functions. How the cell types of striatonigral and striatopallidal neurons are specified to construct these two pathways during development remains elusive. We found that the LIM homeodomain transcription factor Islet-1 (Isl1) was specifically expressed in striatonigral neurons during development. Genetic inactivation of\n                    <jats:italic>Isl1<\/jats:italic>\n                    resulted in increased apoptosis, abnormal differentiation, and aberrant axonal projections of striatonigral neurons. These findings suggest that\n                    <jats:italic>Isl1<\/jats:italic>\n                    plays a key role in specification of striatonigral neurons. Our study provides insights into genetic mechanisms by which basal ganglia circuits are built to function.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1319138111","type":"journal-article","created":{"date-parts":[[2013,12,19]],"date-time":"2013-12-19T02:39:18Z","timestamp":1387420758000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":58,"title":["Dual role for\n                    <i>Islet-1<\/i>\n                    in promoting striatonigral and repressing striatopallidal genetic programs to specify striatonigral cell identity"],"prefix":"10.1073","volume":"111","author":[{"given":"Kuan-Ming","family":"Lu","sequence":"first","affiliation":[{"name":"Institute of Neuroscience, National Yang-Ming University, Taipei, Taiwan 11221, Republic of China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvia M.","family":"Evans","sequence":"additional","affiliation":[{"name":"Skaggs School of Pharmacy and Department of Medicine, University of California, San Diego, La Jolla, CA 92093; 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