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Mouse embryos homozygous for a targeted mutation in the <jats:italic>Zfp36l1<\/jats:italic> locus died mid\u2010gestation and exhibited extraembryonic and intraembryonic vascular abnormalities and heart defects. In the developing placenta, there was a failure of the extraembryonic mesoderm to invaginate the trophoblast layer. The phenotype was associated with an elevated expression of vascular endothelial growth factor (VEGF)\u2010A in the embryos and in embryonic fibroblasts cultured under conditions of both normoxia and hypoxia. VEGF\u2010A overproduction by embryonic fibroblasts was not a consequence of changes in <jats:italic>Vegf\u2010a<\/jats:italic> mRNA stability; instead, we observed enhanced association with polyribosomes, suggesting <jats:italic>Zfp36l1<\/jats:italic> influences translational regulation. These data implicate <jats:italic>Zfp36l1<\/jats:italic>as a negative regulator of <jats:italic>Vegf\u2010a<\/jats:italic> gene activity during development. Developmental Dynamics 235:3144\u20133155, 2006. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/dvdy.20949","type":"journal-article","created":{"date-parts":[[2006,9,29]],"date-time":"2006-09-29T15:57:07Z","timestamp":1159545427000},"page":"3144-3155","source":"Crossref","is-referenced-by-count":97,"title":["The RNA binding protein <i>Zfp36l1<\/i> is required for normal vascularisation and post\u2010transcriptionally regulates VEGF expression"],"prefix":"10.1002","volume":"235","author":[{"given":"Sarah E.","family":"Bell","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria 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