Catalog: | C-EL-1764T |
Product Type: | Test kit |
Size: | 96 tests |
Principle: | Solid Phase Sandwich ELISA |
Conjugation: | HRP |
Species: | Human |
Detection range: | 62.5-4000 pg/mL |
Sensitivity: | 25.24 pg/mL |
Specificity: | Recognizes both recombinant and natural Human DLL4 |
Sample type: | Recombinant protein |
Test type: | Quantitative |
Analysis mode: | ELISA |
Shipping: | This ELISA Kit is shipped at ambient temperature. |
Storage: | 2-8℃ |
Full name: | delta-like 4 (Drosophila) |
Application: | Cancer Drug Targets; Notch Pathway |
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.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.
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