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Flow cytometric analysis of Notch3 expression on human Acute Lymphoblastic Leukemia cell line. Human MOLT-3 cells (ATCC CRL-1552™) were harvested and stained with either PE Mouse IgG1, κ Isotype Control (Cat. No. 556650; dashed line histogram) or PE Anti-Human Notch3 antibody (solid line histogram) at matched concentrations. Fluorescence histograms were derived from gated events with the forward and side-light scattering characteristics of viable MOLT-3 cells. Flow cytometric analysis was performed using a BD FACSCanto™ II Flow Cytometry System.
BD Pharmingen™ PE Mouse Anti-Human Notch3
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- This reagent has been pre-diluted for use at the recommended Volume per Test. We typically use 1 × 10^6 cells in a 100-µl experimental sample (a test).
- An isotype control should be used at the same concentration as the antibody of interest.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
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The MHN3-21 monoclonal antibody specifically binds to an extracellular domain of human Notch3. Notch3 is a type 1 transmembrane glycoprotein receptor and member of the Notch family that includes Notch1-Notch4. The Notch3 precursor is cleaved in the Golgi and presents as a cell surface heterodimeric receptor. The Notch3 receptor can bind to several membrane-bound ligands including Jagged1, Jagged2 and Delta1. Upon ligand binding, Notch3 undergoes proteolytic cleavage that results in the release of the Notch intracellular domain, NICD. NICD translocates to the nucleus where it can form a transcriptional activator complex with various transcription factors. These multimeric complexes either positively or negatively regulate the expression of multiple genes including those that orchestrate many facets of embryonic development and the subsequent functioning of organ systems such as the hematopoietic, immune, nervous and cardiovascular systems. Notch3 is reportedly expressed by monocytes but not by CD34+ cells and most types of normal lymphocytes. Notch3 has also been implicated in the development of T cell neoplasia. Notch3 is expressed in vascular smooth muscle cells and plays a key role in neural development. Mutations in Notch3 have been identified as the underlying cause of CADASIL, a cerebral autosomal dominant disease that is the most common form of hereditary stroke disorder.
Development References (3)
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Haraguchi K, Suzuki T, Koyama N et al. Notch activation induces the generation of functional NK cells from human cord blood CD34-positive cells devoid of IL-15. J Immunol. 2009; 182(10):6168-6178. (Immunogen: Blocking). View Reference
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Joutel A, Corpechot C, Ducros A, et al. Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia. Nature. 1996; 383(6602):707-710. (Biology). View Reference
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Pancewicz J, Nicot C. Current views on the role of Notch signaling and the pathogenesis of human leukemia. BMC Cancer. 2011; 11:502-508. (Biology). View Reference
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