{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T06:49:17Z","timestamp":1790232557088,"version":"4.1.0"},"reference-count":68,"publisher":"The Company of Biologists","issue":"2","license":[{"start":{"date-parts":[[1997,1,15]],"date-time":"1997-01-15T00:00:00Z","timestamp":853286400000},"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":[[1997,1,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:p>Retinoid receptors, which are members of the nuclear hormone receptor superfamily, act as ligand-dependent transcription factors. They mediate the effects of retinoic acid primarily as heterodimers of retinoic acid receptors (RARs) and retinoid X receptors (RXRs). To analyse their function, xRXR \u03b2 synthetic mRNA was injected into Xenopus embryos in combination with normal and mutated xRAR \u03b1 transcripts. Two informative phenotypes are reported here. Firstly, over-expression of xRXR \u03b2 with xRAR \u03b1 results in the formation of ectopic primary neurons. Secondly, blocking retinoid signalling with a mutated xRAR \u03b1 results in a lack of primary neurons. These two phenotypes, from contra-acting manipulations, indicate a role for retinoid signalling during neurogenesis.<\/jats:p>","DOI":"10.1242\/dev.124.2.515","type":"journal-article","created":{"date-parts":[[2021,4,26]],"date-time":"2021-04-26T03:06:09Z","timestamp":1619406369000},"page":"515-523","source":"Crossref","is-referenced-by-count":72,"title":["Retinoid receptors promote primary neurogenesis in <i>Xenopus<\/i>"],"prefix":"10.1242","volume":"124","author":[{"given":"C. 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