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Results showed that DLL3 localized in normal neuroendocrine cells. Considerable upregulation of DLL3 was found in gastrointestinal neuroendocrine carcinoma cell lines. Its silencing caused significant growth inhibition and induction of intrinsic apoptosis. This study suggests that DLL3, expressed in neuroendocrine cells of the gastrointestinal tract, has a pivotal role in gastrointestinal neuroendocrine carcinoma.
DLL3 expression is silenced during hepatocarcinogenesis in association with HBV infection via an epigenetic mechanism
Results showed that DLL3 downregulation attenuated small cell lung cancer (SCLC)-cell proliferation, migration and invasion in a process involving the attenuation of Snail activation. In addition, DLL3 overexpression promoted subcutaneous tumor growth in the mouse models.
The DLL3 expression could be a potential and novel tumor marker for early diagnosis and an independent predictor of poor survival for patients with endometrial cancer
these results reveal that DLL3 is expressed in tumor specimens from most patients with small cell lung cancer
Results indicated that DLL3 expression was silenced in hepatocellular carcinoma (HCC) cells by DNA methylation and was more readily affected by histone acetylation than histone methylation (H3K9me2 or H3K27me3).
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 the para-carcinoma tissues, but positive 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 ligands Dll1 and Dll3 regulates their trafficking and signaling activity
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.
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 signaling through inhibiting Notch signaling in lung cancer.
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 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.
Dll3 targets Notch1 for lysosomal degradation preventing Notch1 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 ligands, including Delta-like1 and 3 and Jagged1 and Jagged2, show distinct expression patterns in the developing and adult brain overlapping that of Notch1
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.
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.
Data demonstrate distinct in vivo functions for DLL1 and DLL3, and suggest that DLL3 does not antagonize DLL1 in the presomitic mesoderm.
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
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
Dll3 are expressed in the developing mouse eye and in retinal progenitor cell.
a complex interplay of E-box binding proteins spatially and temporally regulate Dll3 levels during neural tube development.
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.
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