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

Mouse Monoclonal Antibody

Overview
Brand: Affymetrix eBioscience

Manufacturer Part Number: 17-5787-41

25TEST Anti-Human Notch3 APC

Code: NEW

Additional Details:
Additional Details: Weight: 0.23750kg



Disclaimers: For Research Use Only.

Product Code. 15578126

Quantity Price
1 £ 120.2 / 25 tests
Estimated Shipment date
from Supplier 14-12-2016
Add to basket


Description and Specification

Specification

Antigen Notch3
Applications Flow Cytometry
Clone MHN3-21
Concentration 5μL (0.25μg)/test
Conjugate APC
Format Conjugated
Formulation aqueous buffer, 0.09% sodium azide, may contain carrier protein/stabilizer
Host Species Mouse
Isotype IgG1
Quantity 25 tests
Regulatory Status RUO
Species Reactivity Human
Storage Requirements Store at 2-8°C. Do not freeze. Light-sensitive material.
Primary or Secondary Primary
Monoclonal or Polyclonal Monoclonal

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.