ArticleScientific reports2016
Creb1 regulates late stage mammalian lung development via respiratory epithelial and mesenchymal-independent mechanisms.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Developmental expression of CREB1 and NFATC2 in pig embryos.Molecular biology reports · 2023Article
- Kub3 Deficiency Causes Aberrant Late Embryonic Lung Development in Mice by the FGF Signaling Pathway.International journal of molecular sciences · 2022Article
- CREB1 Transcriptionally Activates LTBR to Promote the NF-Computational and mathematical methods in medicine · 2022Article
- Identification of Novel Biomarkers and Candidate Drug in Ovarian Cancer.Journal of personalized medicine · 2021Article
- Bioinformatic Analyses of Canonical Pathways of TSPOAP1 and its Roles in Human Diseases.Frontiers in molecular biosciences · 2021Article
- Integrating multiomics longitudinal data to reconstruct networks underlying lung development.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Multi-Omics Analysis Identifying Key Biomarkers in Ovarian Cancer.Cancer control : journal of the Moffitt Cancer CenterArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
During mammalian lung development, the morphological transition from respiratory tree branching morphogenesis to a predominantly saccular architecture, capable of air-breathing at birth, is dependent on physical forces as well as molecular signaling by a range of transcription factors including the cAMP response element binding protein 1 (Creb1). Creb1(-/-) mutant mice exhibit complete neonatal lethality consistent with a lack of lung maturation beyond the branching phase. To further define its role in the developing mouse lung, we deleted Creb1 separately in the respiratory epithelium and mesenchyme. Surprisingly, we found no evidence of a morphological lung defect nor compromised neonatal survival in either conditional Creb1 mutant. Interestingly however, loss of mesenchymal Creb1 on a genetic background lacking the related Crem protein showed normal lung development but poor neonatal survival. To investigate the underlying requirement for Creb1 for normal lung development, Creb1(-/-) mice were re-examined for defects in both respiratory muscles and glucocorticoid hormone signaling, which are also required for late stage lung maturation. However, these systems appeared normal in Creb1(-/-) mice. Together our results suggest that the requirement of Creb1 for normal mammalian lung morphogenesis is not dependent upon its expression in lung epithelium or mesenchyme, nor its role in musculoskeletal development.
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