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The Dll3 was rarely detectable in (show PIK3CA ELISA Kits) the (show AKT1 ELISA Kits) para-carcinoma tissues, but positi (show NOTCH1 ELISA Kits)ve in 82.1% of non-small cell cancer tissues.
Both global haplotype and individual haplotype analyses showed that the haplotypes of SNP1/SNP2/SNP3/SNP4/SNP5 did not correlate with the disease (P >0.05). Together, these data suggest that genetic variants of the DLL3 gene are not associated with CS in the Chinese Han population.
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 ELISA Kits) ligands Dll1 (show DLL1 ELISA Kits) and Dll3 regulates their trafficking and signaling activity
Dll3 overexpression promoted PI3K/Akt (show AKT1 ELISA Kits) signaling through inhibiting Notch (show NOTCH1 ELISA Kits) signaling in lung cancer.
O-fucosylation of DLL3 is required for its function during somitogenesis.
Intriguing changes are observed in the cranio-caudal (show CAD ELISA Kits) borders of multifidus muscle in mutant Dll3 and Lfng (show LFNG ELISA Kits) 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 ELISA Kits).
Dll3 targets Notch1 (show NOTCH1 ELISA Kits) for lysosomal degradation preventing Notch1 (show NOTCH1 ELISA Kits) 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 ELISA Kits) ligands, including Delta-like1 and 3 and Jagged1 (show JAG1 ELISA Kits) and Jagged2 (show JAG2 ELISA Kits), show distinct expression patterns in the developing and adult brain overlapping that of Notch1 (show NOTCH1 ELISA Kits)
Data describe the genetic interactions between Dll1 (show DLL1 ELISA Kits), Dll3, Mesp2 (show Mesp2 ELISA Kits) and Psen1 (show PSEN1 ELISA Kits), and the roles of Dll1 (show DLL1 ELISA Kits)- and Dll3-Notch (show NOTCH1 ELISA Kits) pathways, with or without Psen1 (show PSEN1 ELISA Kits), in rostrocaudal patterning.
spondylocostal dysostosis (SCD (show SCD ELISA Kits)) is caused by mutation in Delta-like (show DLK1 ELISA Kits) 3 (DLL3), Mesoderm posterior 2 (MESP2 (show Mesp2 ELISA Kits)), and Lunatic fringe (LFNG (show LFNG ELISA Kits)); three genes that are components of the Notch (show NOTCH1 ELISA Kits) signaling pathway.
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