Brilliant Violet 421™ anti-human CD169 (Sialoadhesin, Siglec-1)

Antibodies Single
Sony
7-239
Flow Cytometry
Mouse IgG1, κ
Human
Human Rhinovirus (HRV14) infected, monocyte derived-DCs
2330085
$203.00

Description

CD169, also known as Siglec-1 and Sialoadhesin (Sn), is a 210 kD type I single membrane-spanning glycoprotein. It is the largest member of the Siglec family, consisting of 1709 amino acids and belonging to the immunoglobulin superfamily. CD169 is expressed by macrophages and dendritic cells. By its affinity to α2,3-linked sialic acid, it is involved in macrophage binding to different cell types such as granulocytes, monocytes, NK, B and T cells. Several CD169 counter receptors, such as CD227 on human breast cancer cells, CD43 on T cells and CD206 on macrophages, have been reported.

Formulation

Phosphate-buffered solution, pH 7.2, containing 0.09% sodium azide and BSA (origin USA).

Recommended Usage

Each lot of this antibody is quality control tested by immunofluorescent staining with flow cytometric analysis. For flow cytometric staining, the suggested use of this reagent is 5 µl per million cells or 5 µl per 100 µl of whole blood. It is recommended that the reagent be titrated for optimal performance for each application.

Brilliant Violet 421™ excites at 405 nm and emits at 421 nm. The standard bandpass filter 450/50 nm is recommended for detection. Brilliant Violet 421™ is a trademark of Sirigen Group Ltd. 



This product is subject to proprietary rights of Sirigen Inc. and is made and sold under license from Sirigen Inc. The purchase of this product conveys to the buyer a non-transferable right to use the purchased product for research purposes only. This product may not be resold or incorporated in any manner into another product for resale. Any use for therapeutics or diagnostics is strictly prohibited. This product is covered by U.S. Patent(s), pending patent applications and foreign equivalents.

References

1. Xiong YS, et al. 2009. Clin. Biochem. 42:1057.
2. Varki A, et al. 2009. Glycoconj J. 26:231.
3. Rempel H, et al. 2008. PLoS One. 3:e1967.
4. Crocker PR, et al. 2001. T