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Our data showed that activation of Respiratory syncytial virus (RSV) stimulated the differentiation of Th17 in airway microenvironment through activation Notch-1/DLL3, which may be associated with the occurrence and development of RSV-induced asthma.
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Structural deformities of the vertebral column and adjacent ribs in the pudgy mouse are caused by mutations in Dll3. Review.
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Dll3 overexpression promoted PI3K/Akt signaling through inhibiting Notch signaling in lung cancer.
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O-fucosylation of DLL3 is required for its function during somitogenesis.
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Intriguing changes are observed in the cranio-caudal borders of multifidus muscle in mutant Dll3 and Lfng models of idiopathic scoliosis.
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Dll3 has a unique function during T-cell development that is distinct from the role played by the other DSL ligands of Notch.
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Dll3 targets Notch1 for lysosomal degradation preventing Notch1 from undergoing post-translational processing.
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Axial skeletal defects caused by mutation in the spondylocostal dysplasia/pudgy gene Dll3 are associated with disruption of the segmentation clock within the presomitic mesoderm.
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DLL3 knockout mice have segmentation and neural defects
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Notch ligands, including Delta-like1 and 3 and Jagged1 and Jagged2, show distinct expression patterns in the developing and adult brain overlapping that of Notch1
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Data describe the genetic interactions between Dll1, Dll3, Mesp2 and Psen1, and the roles of Dll1- and Dll3-Notch pathways, with or without Psen1, in rostrocaudal patterning.
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spondylocostal dysostosis (SCD) is caused by mutation in Delta-like 3 (DLL3), Mesoderm posterior 2 (MESP2), and Lunatic fringe (LFNG); three genes that are components of the Notch signaling pathway.
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Data demonstrate distinct in vivo functions for DLL1 and DLL3, and suggest that DLL3 does not antagonize DLL1 in the presomitic mesoderm.
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study reports that another Notch ligand, Dll3, is expressed in developing hair cells, in a pattern that overlaps that of Dll1 and Jag2; Dll3 may play a role in lateral inhibition similar to that of Dll1 and Jag2
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study shows that genetic interactions between Notch1 and Dll3 result in vertebral segmental defects similar to those seen in congenital scoliosis; craniofacial anomalies not previously observed in Dll3 homozygous animals were identified
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The intracellular region of Notch ligands Dll1 and Dll3 regulates their trafficking and signaling activity
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Dll3 are expressed in the developing mouse eye and in retinal progenitor cell.
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a complex interplay of E-box binding proteins spatially and temporally regulate Dll3 levels during neural tube development.
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Data show that the ubiquitin ligase Huwe1 operates upstream of the N-Myc-DLL3-Notch pathway to control neural stem cell activity and promote neurogenesis.