{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T18:25:59Z","timestamp":1760984759982},"reference-count":69,"publisher":"The Company of Biologists","issue":"Supplement_18","license":[{"start":{"date-parts":[[1994,1,1]],"date-time":"1994-01-01T00:00:00Z","timestamp":757382400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/www.biologists.com\/user-licence-1-1\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1994,1,1]]},"abstract":"<jats:p>Distinct point mutations in the RET proto-oncogene are the cause of the inherited multiple endocrine neoplasia type 2 syndromes (MEN 2), and the congenital gut disorder Hirschsprung disease. The site and type of these mutations suggests that they have differing effects on the activity of the receptor tyrosine kinase encoded by RET. The normal function of the RET receptor tyrosine kinase has yet to be determined. However, this has been investigated by the inactivation of the RET gene in transgenic mice. The devel-opmental abnormalities apparent in these mice, together with the observation that the major tissues affected in MEN 2 and Hirschsprung disease have a common origin in the embryonal neural crest, suggest that RET encodes a receptor for a developmental regulator involved in the genesis of a variety of neural crest derivatives, and in the organogenesis of the kidney.<\/jats:p>","DOI":"10.1242\/jcs.1994.supplement_18.6","type":"journal-article","created":{"date-parts":[[2013,5,24]],"date-time":"2013-05-24T22:12:56Z","timestamp":1369433576000},"page":"43-49","source":"Crossref","is-referenced-by-count":24,"title":["Mutations of the RET proto-oncogene in the multiple endocrine neoplasia type 2 syndromes and Hirschsprung disease"],"prefix":"10.1242","volume":"1994","author":[{"given":"Darrin P.","family":"Smith","sequence":"first","affiliation":[{"name":"1 CRC Human Cancer Genetics Research Group, Department of Pathology, University of Cambridge, Cambridge, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charis","family":"Eng","sequence":"additional","affiliation":[{"name":"1 CRC Human Cancer Genetics Research Group, Department of Pathology, University of Cambridge, Cambridge, UK"},{"name":"2 Division of Medical Oncology, Division of Cancer Epidemiology and Control, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bruce A. 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