Mouse DLL4 (Delta-like protein 4) ELISA Kit (E-EL-M3133)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Mouse DLL4. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Mouse DLL4 and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Mouse DLL4, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Mouse DLL4. You can calculate the concentration of DLL4 in the samples by comparing the OD of the samples to the standard curve.

Delta-Like protein 4 (DLL4) is a type I transmembrane DSL-family Notch ligand. The conserved Notch signaling pathway regulates cell fate and multiple developmental processes, with its dysfunction linked to various diseases. Mice possess four Notch receptors and five ligands. Distinct from Jagged ligands, mouse DLL4 has no extracellular cysteine-rich domain but retains core functional structures, including DSL motif, tandem EGF repeats, a transmembrane region and a short intracellular domain (ICD).Mouse DLL4 specifically binds to endothelial Notch1 and Notch4. Ligand-receptor interaction triggers sequential cleavage by ADAM metalloprotease and γ-secretase, shedding extracellular domains and releasing soluble ICDs. Notch ICD translocates into the nucleus to activate target gene transcription, while DLL4 ICD also mediates independent nuclear signaling. Mouse and human DLL4 share 86% amino acid identity, indicating high cross-species functional conservation.Mouse DLL4 is specifically expressed in arterial endothelium and serves as a key downstream modulator of VEGF-induced angiogenesis. DLL4/Notch signaling suppresses excessive endothelial sprouting and vascular branching to sustain normal vascular development. Heterozygous DLL4 knockout in mice causes severe vascular malformations and embryonic lethality, confirming its indispensable physiological function. Moreover, DLL4 is upregulated in tumor vasculature, and blockade of DLL4/Notch signaling disrupts tumor vascularization and inhibits tumor growth, highlighting its dual roles in physiological and pathological angiogenesis.