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Invitrogen
CD3e Monoclonal Antibody (S4.1), Qdot™ 800
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FIGURE: 1 / 1
CD3e Antibody (Q22149) in Flow
Histogram of gated human lymphocytes labeled with CD3 Mouse Anti-Human mAb (clone S4.1), Qdot® 800 Conjugate. Sample was acquired and analyzed using 405 nm excitation and a 780/60 band pass emission filter using a BD LSR II flow cytometer (BD Biosciences, San Jose, CA).
Product Details
Q22149
Applications
Tested Dilution
Publications
Product Specifications
Published species
Human,
Mouse
Host/Isotype
Mouse
/ IgG2a
Class
Monoclonal
Type
Antibody
Clone
S4.1
Immunogen
Human CD3.
Conjugate
Excitation/Emission Max
300/792 nm
View spectra
Form
Liquid
Storage conditions
4°C
RRID
Target Information
The CD3 complex, composed of gamma, delta, epsilon, and zeta subunits, is essential for the assembly, trafficking, and surface expression of the T cell receptor (TCR) complex. These subunits are structurally related members of the immunoglobulin superfamily and are encoded by closely linked genes on human chromosome 11. CD3 is expressed by thymocytes in a developmentally regulated manner and by all mature T cells, but not on B or NK cells. The CD3 subunits play a crucial role in transducing antigen-recognition signals into the cytoplasm of T cells. The cytoplasmic tails of CD3 subunits contain a double tyrosine-based motif that associates with cytoplasmic signal transduction molecules, mediating T cell activation through the TCR. Crosslinking of the TCR initiates intracellular biochemical pathways that result in cellular activation, proliferation, and potentially growth arrest and cell survival. CD3 is present on 68-82% of normal peripheral blood lymphocytes, 65-85% of thymocytes, and Purkinje cells in the cerebellum. Decreased percentages of T lymphocytes may be observed in some autoimmune diseases. Defects in the CD3 gene are associated with CD3 immunodeficiency, highlighting its importance in immune function and regulation.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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