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Activating\n                    <jats:italic>FGFR<\/jats:italic>\n                    mutations are the underlying\n cause of several craniosynostoses and dwarfism syndromes in humans.\n Here we show that a heterozygotic abrogation of\n                    <jats:italic>FgfR2-exon 9\n (IIIc)<\/jats:italic>\n                    in mice causes a splicing switch, resulting in a\n gain-of-function mutation. The consequences are neonatal growth\n retardation and death, coronal synostosis, ocular proptosis, precocious\n sternal fusion, and abnormalities in secondary branching in several\n organs that undergo branching morphogenesis. This phenotype has strong\n parallels to some Apert's and Pfeiffer's syndrome patients.\n                  <\/jats:p>","DOI":"10.1073\/pnas.071586898","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:36:44Z","timestamp":1027679804000},"page":"3855-3860","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":145,"title":["A splicing switch and gain-of-function mutation in\n                    <i>FgfR2-IIIc<\/i>\n                    hemizygotes causes Apert\/Pfeiffer-syndrome-like phenotypes"],"prefix":"10.1073","volume":"98","author":[{"given":"Mohammad K.","family":"Hajihosseini","sequence":"first","affiliation":[{"name":"Imperial Cancer Research Fund, 44 Lincoln's Inn Fields, London\r WC2A 3PX, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Wilson","sequence":"additional","affiliation":[{"name":"Imperial Cancer Research Fund, 44 Lincoln's Inn 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