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Notch3 Mouse anti-Human, APC, Clone: MHN3-21, eBioscience™

Mouse Monoclonal Antibody

$187.05 - $404.55

Specifications

Antigen Notch3
Clone MHN3-21
Host Species Mouse
Species Reactivity Human
Applications Flow Cytometry
View More Specs

 Disclaimers

For Research Use Only.

Products
Catalog Number Mfr. No. Quantity Price Quantity    

5015211

 
affymetrix
17578741
25 tests Each for $187.05

5015212

 
affymetrix
17578742
100 tests Each for $404.55
Description & Specifications

Specifications

Antigen Notch3
Clone MHN3-21
Host Species Mouse
Species Reactivity Human
Applications Flow Cytometry
Regulatory Status RUO
Conjugate APC
Format Conjugated
Storage Requirements Store at 2-8°C. Do not freeze. Light-sensitive material.
Primary or Secondary Primary
Monoclonal or Polyclonal Monoclonal
Formulation aqueous buffer, 0.09% sodium azide, may contain carrier protein/stabilizer
Concentration 5μL (0.25μg)/test

This MNH3-21 monoclonal antibody reacts with the extracellular domain of human Notch3, one of four members of the Notch family of receptors. Notch receptors are 300kDa single-pass transmembrane proteins. While the extracellular domain contains numerous epidermal growth factor-like repeats for ligand binding, the intracellular domain is involved in cell signaling. Upon binding its membrane-bound ligand (either Delta or Jagged), the Notch receptor undergoes proteolytic cleavage, first by ADAM-family metalloproteases and then by γ-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.

Notch3 expression has been demonstrated on some thymocyte subsets, including CD4-CD8- and CD8SP cells. This Notch receptor is also expressed on vascular smooth muscle and cells of the central nervous system. In addition to its role in stem cell hematopoiesis, Notch3 plays a pivotal role in T cell lineage commitment and thymocyte development. Moreover, Notch3 is overexpressed in human T-cell acute lymphoblastic leukemias (T-ALL) and other cancers. Finally, mutation of Notch3 has been linked to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a CNS degenerative disorder.