Mouse DLL4 (Delta-like protein 4) ELISA Kit

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 gamma-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. Protein function: Involved in the Notch signaling pathway as Notch ligand (PubMed:11134954). Activates NOTCH1 and NOTCH4. Involved in angiogenesis, negatively regulates endothelial cell proliferation and migration and angiogenic sprouting (By similarity). Essential for retinal progenitor proliferation. Required for suppressing rod fates in late retinal progenitors as well as for proper generation of other retinal cell types (PubMed:22323600). During spinal cord neurogenesis, inhibits V2a interneuron fate (By similarity) [The UniProt Consortium]