Target
Mouse DLL4
Synonyms
DLL4 | Delta-like 4 protein | Delta like 4 | Delta-like 4 (Drosophila) | Delta-like 4 homolog | Drosophila Delta homolog 4 | Notch ligand DLL4 | Delta 4 | Delta ligand 4 | Delta-like protein 4 | Delta4 | Hdelta2 | Notch ligand delta-2
Reactivity
Mouse
(tested or 100% immunogen sequence identity)
Specificity
Recognizes mouse Delta-like protein 4 (DLL4), one of the five major ligands of the Notch signalling pathway, which is activated through the binding of specific ligands to the Notch receptors Notch 1-4. The Notch signalling pathway is an evolutionarily conserved pathway in multi-cellular organisms, which is vital for cell-cell communication, important during fundamental developmental and physiological processes, including regulation of cell fate decisions during neuronal, cardiac and endocrine development, stem cell haematopoiesis, thymic T-cell development, and both tumor progression and suppression. Ligation of Notch receptors by their specific ligands, Jagged1 (CD339), Jagged2, Delta like-1 (DLL1), DLL3 and DLL4, on physically adjacent signal receiving cells, induces proteolysis of the receptors by ADAM-family metalloproteases and gamma-secretase complex, within the transmembrane domain, releasing the Notch intracellular domain (NICD) to translocate to the nucleus. Subsequent signal transduction then occurs through either the CSL-NICD-Mastermind complex cascade (canonical pathway), or NF-kappaB-NICD and CSL-NICD-Deltex complex signalling cascades (non-canonical pathway). The canonical pathway inhibits the differentiation of stem cells or progenitor cells, whilst the non-canonical pathway promotes differentiation. DLL4 is expressed by vascular endothelium, and plays a vital role in embryonic vascular development. DLL4 signalling has been shown to play a role in the angiogenesis of clear-cell renal tumors, and pancreatic, bladder and colonic cancer. Studies have shown that DLL4 expression in endothelium cells, can be up-regulated by vascular endothelial growth factor (VEGF) and basic-FGF, and by HIF1 alpha, and that blockade of DLL4 inhibits tumor growth by promoting non-productive angiogenesis. Clone HMD4-2 has been shown to block mouse Notch1-Fc and Notch4-Fc binding to mouse DLL4/CHO cells, and to inhibit subcutaneous tumor growth in mouse tumor models using the murine lung carcinoma cell line KLN205. Removal of Sodium Azide is recommended prior to use in functional assays.