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anti-Human DLL3 Antibodies:
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Human Polyclonal DLL3 Primary Antibody for EIA, IF - ABIN951923
Heuss, Ndiaye-Lobry, Six, Israël, Logeat: The intracellular region of Notch ligands Dll1 and Dll3 regulates their trafficking and signaling activity. in Proceedings of the National Academy of Sciences of the United States of America 2008
Show all 3 references for ABIN951923
Human Polyclonal DLL3 Primary Antibody for EIA, IF - ABIN951924
Yerges, Klei, Cauley, Roeder, Kammerer, Moffett, Ensrud, Nestlerode, Marshall, Hoffman, Lewis, Lang, Barrett-Connor, Ferrell, Orwoll, Zmuda: High-density association study of 383 candidate genes for volumetric BMD at the femoral neck and lumbar spine among older men. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2009
Show all 3 references for ABIN951924
Human Polyclonal DLL3 Primary Antibody for IF, IHC (p) - ABIN656327
Maisenbacher, Han, Obrien, Tracy, Erol, Schaffer, Dormans, Zackai, Kusumi: Molecular analysis of congenital scoliosis: a candidate gene approach. in Human genetics 2005
Show all 3 references for ABIN656327
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 Antibodies) ligands Dll1 (show DLL1 Antibodies) 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 (show CAD Antibodies) borders of multifidus muscle in mutant Dll3 and Lfng (show LFNG Antibodies) 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 Antibodies).
Dll3 targets Notch1 (show NOTCH1 Antibodies) for lysosomal degradation preventing Notch1 (show NOTCH1 Antibodies) 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 Antibodies) ligands, including Delta-like1 and 3 and Jagged1 (show JAG1 Antibodies) and Jagged2 (show JAG2 Antibodies), show distinct expression patterns in the developing and adult brain overlapping that of Notch1 (show NOTCH1 Antibodies)
Data describe the genetic interactions between Dll1 (show DLL1 Antibodies), Dll3, Mesp2 (show Mesp2 Antibodies) and Psen1 (show PSEN1 Antibodies), and the roles of Dll1 (show DLL1 Antibodies)- and Dll3-Notch (show NOTCH1 Antibodies) pathways, with or without Psen1 (show PSEN1 Antibodies), in rostrocaudal patterning.
spondylocostal dysostosis (SCD (show SCD Antibodies)) is caused by mutation in Delta-like (show DLK1 Antibodies) 3 (DLL3), Mesoderm posterior 2 (MESP2 (show Mesp2 Antibodies)), and Lunatic fringe (LFNG (show LFNG Antibodies)); three genes that are components of the Notch (show NOTCH1 Antibodies) signaling pathway.
Data demonstrate distinct in vivo functions for DLL1 (show DLL1 Antibodies) and DLL3, and suggest that DLL3 does not antagonize DLL1 (show DLL1 Antibodies) 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