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Nuclear factor I-B (Nfib) deficient mice have severe lung hypoplasia

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Mallo,  Moisés
Max Planck Society;

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Shimizu,  Takehiko
Department of Developmental Biology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Schrewe,  Heinrich
Department of Developmental Biology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Gründer, A., Ebel, T. T., Mallo, M., Schwarzkopf, G., Shimizu, T., Sippel, A. E., et al. (2002). Nuclear factor I-B (Nfib) deficient mice have severe lung hypoplasia. Mechanisms of Development, 112(1-2), 69-77.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-9661-A
Abstract
Binding sites for transcription factor nuclear factor one (NFI) proteins, encoded by four genes in the mouse, have been characterized from many tissue-specific genes. NFI genes are expressed in unique but overlapping patterns in embryonic and in adult tissues. Nfib is highly expressed in the embryonic lung. Here we show that Nfib null mutants die early postnatally and display severe lung hypoplasia. Heterozygotes do survive, but exhibit delayed pulmonary differentiation. Expression of transforming growth factor β 1 (TGF-β1) and sonic hedgehog (Shh) is not down-regulated in mutant lung epithelium at late stages of morphogenesis, which may result in incomplete lung maturation. Our study demonstrates that Nfib is essential for normal lung development, and suggests that it could be involved in the pathogenesis of respiratory distress syndromes in humans. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.