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DLL3 was silenced by methylation in human human hepatocellular carcinoma and it negatively regulates the growth of human hepatocellular carcinoma cells.
We suggest that the three human DLL3 mutations associated with spondylocostal dysplasia are also functionally equivalent to the Dll3(neo) null allele in mice.
mutations in DLL3 cause a consistent pattern of abnormal vertebral segmentation in spondylocostal dysostosis
no novel or previously described mutations are present in our cohort, indicating that DLL3 mutations may not be a major cause of congenital scoliosis.
The intracellular region of Notch (show NOTCH1 Proteins) ligands Dll1 (show DLL1 Proteins) and Dll3 regulates their trafficking and signaling activity
O-fucosylation of DLL3 is required for its function during somitogenesis.
Intriguing changes are observed in the cranio-caudal borders of multifidus muscle in mutant Dll3 and Lfng (show LFNG Proteins) models of idiopathic scoliosis.
Dll3 has a unique function during T-cell development that is distinct from the role played by the other DSL ligands of Notch (show NOTCH1 Proteins).
Dll3 targets Notch1 (show NOTCH1 Proteins) for lysosomal degradation preventing Notch1 (show NOTCH1 Proteins) from undergoing post-translational processing.
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.
DLL3 knockout mice have segmentation and neural defects
Notch (show NOTCH1 Proteins) ligands, including Delta-like1 and 3 and Jagged1 (show JAG1 Proteins) and Jagged2 (show JAG2 Proteins), show distinct expression patterns in the developing and adult brain overlapping that of Notch1 (show NOTCH1 Proteins)
Data describe the genetic interactions between Dll1 (show DLL1 Proteins), Dll3, Mesp2 (show Mesp2 Proteins) and Psen1 (show PSEN1 Proteins), and the roles of Dll1 (show DLL1 Proteins)- and Dll3-Notch (show NOTCH1 Proteins) pathways, with or without Psen1 (show PSEN1 Proteins), in rostrocaudal patterning.
spondylocostal dysostosis (SCD (show SCD Proteins)) is caused by mutation in Delta-like (show DLK1 Proteins) 3 (DLL3), Mesoderm posterior 2 (MESP2 (show Mesp2 Proteins)), and Lunatic fringe (LFNG (show LFNG Proteins)); three genes that are components of the Notch (show NOTCH1 Proteins) signaling pathway.
Data demonstrate distinct in vivo functions for DLL1 (show DLL1 Proteins) and DLL3, and suggest that DLL3 does not antagonize DLL1 (show DLL1 Proteins) in the presomitic mesoderm.
This gene encodes a member of the delta protein ligand family. This family functions as Notch ligands that are characterized by a DSL domain, EGF repeats, and a transmembrane domain. Mutations in this gene cause autosomal recessive spondylocostal dysostosis 1. Two transcript variants encoding distinct isoforms have been identified for this gene.
delta-like protein 3
, drosophila Delta homolog 3