All DLL4 reagents are produced in house and quality controlled, including 9 DLL4 Antibody, 4 DLL4 ELISA, 27 DLL4 Gene, 5 DLL4 Lysate, 5 DLL4 Protein, 2 DLL4 qPCR. All DLL4 reagents are ready to use.
Recombinant DLL4 proteins are expressed by HEK293 Cells with fusion tags as C-His, C-cleavage, C-human IgG1-Fc.
DLL4antibodies are validated with different applications, which are ELISA(Cap), WB, ELISA, ELISA(Det).
DLL4cDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each DLL4 of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
DLL4ELISA Kit are quality controlled by 8 internation QC standard which guarantee every ELISA Kit with high quality.
Delta-like protein 4 (DLL4, Delta4), a type I membrane-bound Notch ligand, is one of five known Notch ligands in mammals and interacts predominantly with Notch 1, which has a key role in vascular development. Recent studies yield substantial insights into the role of DLL4 in angiogenesis. DLL4 is induced by vascular endothelial growth factor (VEGF) and acts downstream of VEGF as a 'brake' on VEGF-induced vessel growth, forming an autoregulatory negative feedback loop inactivating VEGF. DLL4 is downstream of VEGF signaling and its activation triggers a negative feedback that restrains the effects of VEGF. Attenuation of DLL4/Notch signaling results in chaotic vascular network with excessive branching and sprouting. DLL4 is widely distributed in tissues other than vessels including many malignancies. Furthermore, the molecule is internalized on binding its receptor and often transported to the nucleus. In pathological conditions, such as cancer, DLL4 is up-regulated strongly in the tumour vasculature. Blockade of DLL4-mediated Notch signaling strikingly increases nonproductive angiogenesis, but significantly inhibits tumor growth in preclinical mouse models. In preclinical studies, blocking of DLL4/Notch signaling is associated with a paradoxical increase in tumor vessel density, yet causes marked growth inhibition due to functionally defective vasculature. Thus, DLL4 blockade holds promise as an additional strategy for angiogenesis-based cancer therapy.