DLL4 ELISA Kit, Human General Information
DLL4 ELISA Kit, Human
Solid Phase Sandwich ELISA (quantitative)
Recognizes both recombinant and natural Human DLL4
The recovery of Human DLL4 spiked to different levels throughout the range of the assay in related matrices was evaluated.
||Average % Recovery
||Recovery of detected
1. 96 well microplate coated with Capture Antibody
2. Detection Antibody conjugated to HRP
4. Wash Buffer Concentrate
5. Dilution Buffer Concentrate
6. Color Reagent A
7. Color Reagent B
8. Stop Solution
This DLL4 ELISA Kit, Human is an enzyme-linked immunosorbent assay for the quantitative measurement of Human DLL4 protein in Recombinant protein . It contains recombinant Human DLL4, and antibodies raised against the recombinant protein. This ELISA kit is complete and ready-to-use.
This ELISA Kit is shipped at ambient temperature.
Unopened Kit: Store at 2 - 8℃
Opened/Reconstituted Reagents: Please refer to CoA
DLL4 ELISA Kit, Human Images
This standard curve is only for demonstration purposes. A standard curve should be generated for each assay.
This assay recognizes recombinant Human DLL4. The factors listed above were prepared at 50 ng/mL in dilution buffer and assayed for cross-reactivity. No cross-reactivity was observed.
DLL4 ELISA Kit, Human Alternative Names
Delta-like 4 ELISA Kit, Human;hdelta2 ELISA Kit, Human
DLL4 Background Information
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.
delta-like 4 (Drosophila)
Yan M, et al. (2007) Delta-like 4/Notch signaling and its therapeutic implications. Clin Cancer Res. 13(24): 7243-6.Sainson RC, et al. (2007) Anti-Dll4 therapy: can we block tumour growth by increasing angiogenesis? Trends Mol Med. 13(9): 389-95.Martinez JC, et al. (2009) Nuclear and membrane expression of the angiogenesis regulator delta-like ligand 4 (DLL4) in normal and malignant human tissues. Histopathology. 54(5): 598-606.Li JL, et al. (2010) Targeting DLL4 in tumors shows preclinical activity but potentially significant toxicity. Future Oncol. 6(7): 1099-103.