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Catalog Number Size Price
LS-C188303-0.1 0.1 mg (0.1 mg/ml) $444 
NOTCH1 Antibody - Flow cytometry of mouse thymocytes with Mouse anti-Mouse NOTCH-1:FITC This image was taken for the unconjugated form of this product. Other forms have not been tested.

Monoclonal Mouse anti‑Mouse NOTCH1 Antibody (clone mN1A, FITC, IHC) LS‑C188303

Monoclonal Mouse anti‑Mouse NOTCH1 Antibody (clone mN1A, FITC, IHC) LS‑C188303

Antibody:
NOTCH1 Mouse anti-Mouse Monoclonal (FITC) (mN1A) Antibody
Application:
IHC, IHC-Fr, Flo
Reactivity:
Mouse
Format:
FITC, Unmodified
Other formats:
Price
Catalog Number
$444
LS-C188303-0.1
Toll Free North America
(800) 227-6666
For Research Use Only

Overview

Antibody:
NOTCH1 Mouse anti-Mouse Monoclonal (FITC) (mN1A) Antibody
Application:
IHC, IHC-Fr, Flo
Reactivity:
Mouse
Format:
FITC, Unmodified
Other formats:

Specifications

Description
NOTCH1 antibody LS-C188303 is an FITC-conjugated mouse monoclonal antibody to mouse NOTCH1. Validated for Flow and IHC.
Target
Mouse NOTCH1
Synonyms
NOTCH1 | Notch 1 | TAN1
Host
Mouse
Reactivity
Mouse (tested or 100% immunogen sequence identity)
Clonality
IgG1 Monoclonal
Clone
mN1A
Conjugations
FITC. Also available Unconjugated or conjugated with RPE.
Purification
Protein G purified
Modifications
Unmodified
Immunogen
Synthetic peptide corresponding to cdc10-NCR region within mouse Notch1
Specificity
Recognizes Notch 1, one of the four major transmembrane receptors (Notch 1-4) of the Notch signalling pathway, which is activated through binding to DSL domain-containing membrane-bound specific ligands. 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. Notch 1 is expressed in a range of cells including hematopoietic cells in mouse fetal liver, adult thymus and bone marrow. Notch 1 signalling plays a role in follicular differentiation, tissue homeostasis, and in both CD4+ and CD8+ cell maturation in the thymus. Studies have also implicated Notch 1 in the regulation of lymphopoiesis, myelopoiesis, and neurogenesis.
Applications
  • IHC
  • IHC - Frozen
  • Flow Cytometry (1:1 - 1:10)
  • Applications tested for the base form of this product only
Performing IHC? See our complete line of Immunohistochemistry Reagents including antigen retrieval solutions, blocking agents ABC Detection Kits and polymers, biotinylated secondary antibodies, substrates and more.
Usage
The applications listed have been tested for the unconjugated form of this product. Other forms have not been tested.
Presentation
PBS, 0.09% Sodium Azide, 1% BSA
Storage
Store at 4°C or at -20°C. Store undiluted. Avoid freeze-thaw cycles. Microcentrifugation recommended if solution contains precipitate.
Restrictions
For research use only. Intended for use by laboratory professionals.
Guarantee
This antibody carries the LSBio 100% Guarantee.
LSBio Guarantee
About NOTCH1
P46531 NM_017617 NP_060087.3

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To request an SDS/MSDS form for this product, please contact our Technical Support department at:

Technical.Support@LSBio.com

Requested From: United States
Date Requested: 11/22/2024