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ErbB4 deletion leads to changes in lung function and structure similar to bronchopulmonary dysplasia.
Neuregulin is an important growth factor in fetal surfactant synthesis, and downregulation of its receptor, ErbB4, impairs fetal surfactant synthesis. We hypothesized that pulmonary ErbB4 deletionExpand
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The ErbB4 receptor in fetal rat lung fibroblasts and epithelial type II cells.
ErbB receptors are important regulators of fetal organ development, including the fetal lung. They exhibit diversity in signaling potential, acting through homo- and heterodimers to cause differentExpand
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ErbB receptors in fetal endothelium--a potential linkage point for inflammation-associated neonatal disorders.
OBJECTIVE ErbB receptors and their ligands play crucial roles in development. During late gestation, they might also be involved in the pathogenesis of prematurity-associated disorders. ErbB receptorExpand
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ErbB receptor dimerization, localization, and co‐localization in mouse lung type II epithelial cells
ErbB receptors are crucial for embryonic neuronal and cardiac development. ErbB receptor ligands neuregulin (NRG) and epidermal growth factor (EGF) play a major role in the developing lung,Expand
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Neuregulin receptor ErbB4 functions as a transcriptional cofactor for the expression of surfactant protein B in the fetal lung.
Sufficient pulmonary surfactant production is required for the fetal-neonatal transition, especially in preterm infants. Neuregulin (NRG) and its transmembrane receptor ErbB4 positively regulate theExpand
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Reduced airway inflammation in CD26/DPP4‐deficient F344 rats is associated with altered recruitment patterns of regulatory T cells and expression of pulmonary surfactant proteins
Introduction CD26 is highly expressed on lung epithelial cells as well as on immune cells. Ovalbumin (OVA)‐induced airway inflammation induces a further increase of CD26 expression. CD26‐deficientExpand
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ErbB4 regulates fetal surfactant phospholipid synthesis in primary fetal rat type II cells.
Insufficient fetal surfactant production leads to respiratory distress syndrome among preterm infants. Neuregulin signals the onset of fetal surfactant phospholipid synthesis through formation ofExpand
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ErbB4 regulates the timely progression of late fetal lung development.
The ErbB4 receptor has an important function in fetal lung maturation. Deletion of ErbB4 leads to alveolar hypoplasia and hyperreactive airways similar to the changes in bronchopulmonary dysplasiaExpand
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Presenilin-1 processing of ErbB4 in fetal type II cells is necessary for control of fetal lung maturation.
Maturation of pulmonary fetal type II cells to initiate adequate surfactant production is crucial for postnatal respiratory function. Little is known about specific mechanisms of signal transductionExpand
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Lipopolysaccharide-induced injury is more pronounced in fetal transgenic ErbB4-deleted lungs.
Pulmonary ErbB4 deletion leads to a delay in fetal lung development, alveolar simplification, and lung function disturbances in adult mice. We generated a model of intrauterine infection in ErbB4Expand
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