DLL4 (delta-like 4) Monoclonal Antibody (HMD4-1), Functional Grade, eBioscience™, Invitrogen™

Description

Description: This HMD4-1 monoclonal antibody reacts with the extracellular domain of mouse Delta-like 4, one of five type I transmembrane proteins that serves as a Notch receptor ligand. Upon binding the Notch receptor (e.g., Notch 1-4), Delta-like 4 undergoes proteolytic cleavage, first by ADAM-family metalloproteases and then by gamma-secretase. The second cleavage event releases the Notch intracellular domain (NICD), which subsequently translocates into the nucleus, heterodimerizes with the DNA-binding protein RBP-J, recruits co-activator molecules, and ultimately activates transcription. Delta-like 4 is expressed by thymic lymphoid and stromal cells, as well as macrophages and dendritic cells in the spleen. This molecule is also expressed in non-immune cells, including vascular smooth muscle and endothelial cells. Delta-like 4 plays a role in T cell development, regulation of experimental autoimmune encephalomyelitis, and the formation of mature vasculature. The HMD4-1 monoclonal antibody has been reported to have blocking activity and crossreact to rat. Applications Reported: The HMD4-1 antibody has been reported for use in functional assays. Applications Tested: This HMD4-1 antibody has been tested by flow cytometric analysis of mouse Delta-like 4-transfected cells. This can be used at less than or equal to 0.06 μg per test. A test is defined as the amount (μg) of antibody that will stain a cell sample in a final volume of 100 μL.

Delta-like ligand 4 (DLL4), also know as Delta-4, is a homologue of the Drosophila delta protein, and functions as a transmembrane bound ligand to the notch receptor Notch1. DLL4 is expressed in the vasculature and plays a critical role in vascular development. It is induced by vascular endothelial growth factor (VEGF), as a negative feedback regulator to regulate angiogenic sprouting and promote the formulation of a differentiated vascular network. DLL4 has been found to be strongly expressed in tumor vessels of clear-cell renal tumors and bladder cancer, and inhibition of DLL4 results in increased vascular proliferation but defective maturation. This in turn leads to a decrease in tumor growth, with no apparent toxicity.