ArticleProceedings of the National Academy of Sciences of the United States of America2009
NPAS3 is a trachealess homolog critical for lung development and homeostasis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Population genomics of sika deer reveals recent speciation and genetic selective signatures during evolution and domestication.BMC genomics · 2025Article
- The Human Accelerated Region HAR202 Controls NPAS3 Expression in the Developing Forebrain Displaying Differential Enhancer Activity Between Modern and Archaic Human Sequences.Molecular biology and evolution · 2024Article
- Mechanisms of NaFrontiers in physiology · 2022Review
- Dynamic adult tracheal plasticity drives stem cell adaptation to changes in intestinal homeostasis in Drosophila.Nature cell biology · 2021Article
- Pathogenic variants in E3 ubiquitin ligase RLIM/RNF12 lead to a syndromic X-linked intellectual disability and behavior disorder.Molecular psychiatry · 2019Article
- Glial response to hypoxia in mutants of NPAS1/3 homolog Trachealess through Wg signaling to modulate synaptic bouton organization.PLoS genetics · 2019Article
- Molecular analysis of NPAS3 functional domains and variants.BMC molecular biology · 2018Article
- Neuronal PAS Domain Proteins 1 and 3 Are Master Regulators of Neuropsychiatric Risk Genes.Biological psychiatry · 2017Article
- Parametric Linkage Analysis Identifies Five Novel Genome-Wide Significant Loci for Familial Lung Cancer.Human heredity · 2016Article
- Lower NPAS3 expression during the later stages of abnormal lung development in rat congenital diaphragmatic hernia.Pediatric surgery international · 2015Article
- Genome-Wide Association Study Identifies Novel Loci Associated With Diisocyanate-Induced Occupational Asthma.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Lung development: orchestrating the generation and regeneration of a complex organ.Development (Cambridge, England) · 2014Review
- Article
- Rank-based genome-wide analysis reveals the association of ryanodine receptor-2 gene variants with childhood asthma among human populations.Human genomics · 2013Article
- Comparative molecular developmental aspects of the mammalian- and the avian lungs, and the insectan tracheal system by branching morphogenesis: recent advances and future directions.Frontiers in zoology · 2012Article
- Trachealess (Trh) regulates all tracheal genes during Drosophila embryogenesis.Developmental biology · 2011Article
- NPAS3 demonstrates features of a tumor suppressive role in driving the progression of Astrocytomas.The American journal of pathology · 2011Article
- Embryonic multipotent progenitors remodel the Drosophila airways during metamorphosis.Development (Cambridge, England) · 2010Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Trachealess (Trh) is a PAS domain transcription factor regulating Drosophila tracheogenesis. No other Trh homolog has been associated with a respiratory phenotype. Seeking homolog(s) regulating lung development, we screened murine genomic DNA using trh oligonucleotides, identifying only Npas3. Npas3 mRNA peaks in lung from E10.5 to E13.5, verified by sequencing, with immunostaining in airway epithelial cells. Npas3-null mice have reduced lung branching morphogenesis but are viable prenatally. Npas3-null newborns die in respiratory distress, with diminished alveolarization, decreased Shh, Fgf9, Fgf10, and Bmp4 mRNAs, and increased Spry2, consistent with reduced FGF signaling. Exogenous FGF10 rescues branching morphogenesis in Npas3-null lungs. In promoter reporter assays, NPAS3 directly upregulates Shh and represses Spry2. Npas3(+/-) mice have a milder lung phenotype, surviving postnatally, but develop emphysema and airways hyperreactivity. Therefore, absence of a developmentally expressed transcription factor can alter downstream gene expression and multiple signaling pathways in organogenesis. NPAS3 haploinsufficiency may also lead to emphysema and asthma.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.