Skip to Content
Merck
All Photos(1)

Key Documents

SAB4700276

Sigma-Aldrich

Monoclonal Anti-CD16 antibody produced in mouse

clone MEM-154, purified immunoglobulin, buffered aqueous solution

Synonym(s):

Anti-FCGR3A, Anti-FcγRIII

Sign Into View Organizational & Contract Pricing
All Photos(1)

About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

MEM-154, monoclonal

form

buffered aqueous solution

species reactivity

human

concentration

1 mg/mL

technique(s)

flow cytometry: suitable

isotype

IgG1

NCBI accession no.

NM_000569.6

UniProt accession no.

P08637

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

Gene Information

human ... FCGR3A(2214)

General description

The antibody MEM-154 reacts with the epitope on CD16 antigen that residing in proximity to FG loop (probably BC or C′E loop). CD16 is a low affinity receptor for aggregated IgG (FcgammaRIII antigen). The antibody MEM-154 reacts with CD16+ granulocytes.

Immunogen

Human granulocytes

Application

The reagent is designed for Flow Cytometry analysis of human blood cells using 5-10 μg/mL of sample.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physical form

Solution in Tris buffered saline, pH 8.0, with 15 mM sodium azide.

Not finding the right product?  

Try our Product Selector Tool.

Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

Already Own This Product?

Find documentation for the products that you have recently purchased in the Document Library.

Visit the Document Library

Giovanni F Torelli et al.
Haematologica, 99(7), 1248-1254 (2014-03-25)
In this study, we aimed to investigate the pathways of recognition of acute lymphoblastic leukemia blasts by natural killer cells and to verify whether differences in natural killer cell activating receptor ligand expression among groups defined by age of patients
Eri Shimura et al.
Biochemical and biophysical research communications, 453(1), 1-6 (2014-09-11)
IL-17RA is a shared receptor subunit for several cytokines of the IL-17 family, including IL-17A, IL-17C, IL-17E (also called IL-25) and IL-17F. It has been shown that mice deficient in IL-17RA are more susceptible to sepsis than wild-type mice, suggesting
Megan M Tu et al.
Cancer research, 74(14), 3684-3694 (2014-05-08)
According to the missing-self hypothesis, natural killer (NK) cells survey for target cells that lack MHC-I molecules. The Ly49 receptor family recognizes loss of MHC-I and is critical for educating NK cells, conferring the ability to eliminate transformed or infected
Britnie R James et al.
Cancer immunology, immunotherapy : CII, 63(11), 1213-1227 (2014-08-22)
Tumor progression occurs through the modulation of a number of physiological parameters, including the development of immunosuppressive mechanisms to prevent immune detection and response. Among these immune evasion mechanisms, the mobilization of myeloid-derived suppressor cells (MDSC) is a major contributor
Allen Y Chung et al.
Cancer research, 74(19), 5377-5385 (2014-09-18)
Immune dysregulation drives the pathogenesis of chronic inflammatory, autoimmune, and dysplastic disorders. While often intended to address localized pathology, most immune modulatory therapies are administered systemically and carry inherent risk of multiorgan toxicities. Here, we demonstrate, in a murine model
View All Related Papers

Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.

Contact Technical Service