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抗Human DLL3 抗体:
抗Mouse (Murine) DLL3 抗体:
抗Rat (Rattus) DLL3 抗体:
Human Polyclonal DLL3 Primary Antibody for ELISA, WB - ABIN2473315
Bray: Notch signalling: a simple pathway becomes complex. in Nature reviews. Molecular cell biology 2006
our results indicated epidermal growth factor-like domain multiple 7 protein participates in growth hormone-secreting pituitary adenoma proliferation and invasion regulation via Notch2/DLL3 signaling pathway. These findings raised the possibility that epidermal growth factor-like domain multiple 7 protein might serve as a useful biomarker to assess growth hormone-secreting pituitary adenoma invasion and prognosis
The Dll3 was rarely detectable in (显示 PIK3CA 抗体) the (显示 AKT1 抗体) para-carcinoma tissues, but positi (显示 NOTCH1 抗体)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 (显示 NOTCH1 抗体) ligands Dll1 (显示 DLL1 抗体) and Dll3 regulates their trafficking and signaling activity
Structural deformities of the vertebral column and adjacent ribs in the pudgy mouse are caused by mutations in Dll3. Review.
Dll3 overexpression promoted PI3K/Akt (显示 AKT1 抗体) signaling through inhibiting Notch (显示 NOTCH1 抗体) signaling in lung cancer.
O-fucosylation of DLL3 is required for its function during somitogenesis.
Intriguing changes are observed in the cranio-caudal (显示 CAD 抗体) borders of multifidus muscle in mutant Dll3 and Lfng (显示 LFNG 抗体) 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 (显示 NOTCH1 抗体).
Dll3 targets Notch1 (显示 NOTCH1 抗体) for lysosomal degradation preventing Notch1 (显示 NOTCH1 抗体) 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 (显示 NOTCH1 抗体) ligands, including Delta-like1 and 3 and Jagged1 (显示 JAG1 抗体) and Jagged2 (显示 JAG2 抗体), show distinct expression patterns in the developing and adult brain overlapping that of Notch1 (显示 NOTCH1 抗体)
Data describe the genetic interactions between Dll1 (显示 DLL1 抗体), Dll3, Mesp2 (显示 Mesp2 抗体) and Psen1 (显示 PSEN1 抗体), and the roles of Dll1 (显示 DLL1 抗体)- and Dll3-Notch (显示 NOTCH1 抗体) pathways, with or without Psen1 (显示 PSEN1 抗体), in rostrocaudal patterning.
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