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The Dll3 was rarely detectable in (Montrer PIK3CA Kits ELISA) the (Montrer AKT1 Kits ELISA) para-carcinoma tissues, but positi (Montrer NOTCH1 Kits ELISA)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 (Montrer NOTCH1 Kits ELISA) ligands Dll1 (Montrer DLL1 Kits ELISA) and Dll3 regulates their trafficking and signaling activity
Dll3 overexpression promoted PI3K/Akt (Montrer AKT1 Kits ELISA) signaling through inhibiting Notch (Montrer NOTCH1 Kits ELISA) signaling in lung cancer.
O-fucosylation of DLL3 is required for its function during somitogenesis.
Intriguing changes are observed in the cranio-caudal (Montrer CAD Kits ELISA) borders of multifidus muscle in mutant Dll3 and Lfng (Montrer LFNG Kits ELISA) 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 (Montrer NOTCH1 Kits ELISA).
Dll3 targets Notch1 (Montrer NOTCH1 Kits ELISA) for lysosomal degradation preventing Notch1 (Montrer NOTCH1 Kits ELISA) 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 (Montrer NOTCH1 Kits ELISA) ligands, including Delta-like1 and 3 and Jagged1 (Montrer JAG1 Kits ELISA) and Jagged2 (Montrer JAG2 Kits ELISA), show distinct expression patterns in the developing and adult brain overlapping that of Notch1 (Montrer NOTCH1 Kits ELISA)
Data describe the genetic interactions between Dll1 (Montrer DLL1 Kits ELISA), Dll3, Mesp2 (Montrer Mesp2 Kits ELISA) and Psen1 (Montrer PSEN1 Kits ELISA), and the roles of Dll1 (Montrer DLL1 Kits ELISA)- and Dll3-Notch (Montrer NOTCH1 Kits ELISA) pathways, with or without Psen1 (Montrer PSEN1 Kits ELISA), in rostrocaudal patterning.
spondylocostal dysostosis (SCD (Montrer SCD Kits ELISA)) is caused by mutation in Delta-like (Montrer DLK1 Kits ELISA) 3 (DLL3), Mesoderm posterior 2 (MESP2 (Montrer Mesp2 Kits ELISA)), and Lunatic fringe (LFNG (Montrer LFNG Kits ELISA)); three genes that are components of the Notch (Montrer NOTCH1 Kits ELISA) 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