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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Abnormal lung development and cleft palate in mice lacking TGF-beta 3 indicates defects of epithelial-mesenchymal interaction.

A broad spectrum of biological activities has been proposed for transforming growth factor-beta 3 ( TGF-beta 3). To study TGF-beta 3 function in development, TGF-beta 3 null mutant mice were generated by gene-targeting. Within 20 hours of birth, homozygous TGF-beta 3-/- mice die with unique and consistent phenotypic features including delayed pulmonary development and defective palatogenesis. Unlike other null mutants with cleft palate, TGF-beta 3-/- mice lack other concomitant craniofacial abnormalities. This study demonstrates an essential function for TGF-beta 3 in the normal morphogenesis of palate and lung, and directly implicates this cytokine in mechanisms of epithelial-mesenchymal interaction.[1]

References

  1. Abnormal lung development and cleft palate in mice lacking TGF-beta 3 indicates defects of epithelial-mesenchymal interaction. Kaartinen, V., Voncken, J.W., Shuler, C., Warburton, D., Bu, D., Heisterkamp, N., Groffen, J. Nat. Genet. (1995) [Pubmed]
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