Anti-DLL4 Antibody (Rabbit Polyclonal antibody) General Information
Reacts with: Human
Recombinant Human DLL4 protein (Catalog#10171-H08H)
Produced in rabbits immunized with purified, recombinant Human DLL4 / Delta4 extracellular domain (rh DLL4; Catalog#10171-H08H; NP_061947.1; Met 1-Pro 524). DLL4 specific IgG was purified by human DLL4 affinity chromatography.
Polyclonal Rabbit IgG
Protein A & Antigen Affinity
0.2 μm filtered solution in PBS
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.
Please Note: Optimal concentrations/dilutions should be determined by the end user.
Anti-DLL4 Antibody: Alternative Names
Anti-Delta-like 4 Antibody; Anti-hdelta2 Antibody
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.
Successfully added to cart Please enter catalog numberSubmitted successfullyNetwork ErrorPlease enter your company namePlease enter your namePlease enter your emailPlease enter a valid email addressPlease enter some message