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SRP8040

Sigma-Aldrich

LAG-3 (human): FC (human)

recombinant, expressed in CHO cells, >99% (SDS-PAGE)

Synonym(s):

FDC Protein, Lymphocyte activation gene-3, PC cell-derived growth factor

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About This Item

UNSPSC Code:
12352200
NACRES:
NA.32

biological source

human

recombinant

expressed in CHO cells

assay

>99% (SDS-PAGE)

form

liquid

mol wt

~80 kDa by SDS-PAGE

packaging

pkg of 50 μg

concentration

≥0.2 mg/mL

impurities

<0.1 EU/μg endotoxin, tested

color

clear

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... LAG3(3902)

General description

LAG3 (lymphocyte activation gene 3) is an inhibitory CD4 (cluster of differentiation)-related molecule, and is expressed by activated CD4+ and CD8+ T cells.

Biochem/physiol Actions

LAG3 (lymphocyte activation gene 3) is a negative regulator of T-cell proliferation where it suppresses T-cell receptor (TCR)-mediated calcium fluxes and modulates the memory T-cell pool size. It is a CD4 (cluster of differentiation) homolog that functions as a ligand for MHC (major histocompatibility complex) II. Membrane expression of LAG3 modulates the suppressive function of Tregs (T-regulatory) both in vivo and in vitro. HIV-1 (human immunodeficiency virus) infection results in significant increase in LAG3 peripheral blood and lymph node expression, which is exhibited on both CD4+ and CD8+ T cells, and this is linked with disease progression. In melanoma, this protein is responsible for TLR (Toll-like receptor)-independent activation of plasmacytoid dendritic cells (pDCs) at tumor sites, which is partially implicated in driving an immune-suppressive environment.

Physical form

Solution in PBS.

Other Notes

The sequence coding for the 4 extracellular Ig-like domains of human LAG-3 (D1-D4) is fused to the Fc portion of human IgG1.

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Tumor-infiltrating NY-ESO-1-specific CD8+ T cells are negatively regulated by LAG-3 and PD-1 in human ovarian cancer.
Matsuzaki J et al
Proceedings of the National Academy of Sciences of the USA, 107(17), 7875-7880 (2010)
Ching-Tai Huang et al.
Immunity, 21(4), 503-513 (2004-10-16)
Regulatory T cells (Tregs) limit autoimmunity but also attenuate the magnitude of antipathogen and antitumor immunity. Understanding the mechanism of Treg function and therapeutic manipulation of Tregs in vivo requires identification of Treg-selective receptors. A comparative analysis of gene expression
Chiara Camisaschi et al.
The Journal of investigative dermatology, 134(7), 1893-1902 (2014-01-21)
Plasmacytoid dendritic cells (pDCs) at tumor sites are often tolerogenic. Although pDCs initiate innate and adaptive immunity upon Toll-like receptor (TLR) triggering by pathogens, TLR-independent signals may be responsible for pDC activation and immune suppression in the tumor inflammatory environment.
Xiaoling Tian et al.
Journal of immunology (Baltimore, Md. : 1950), 194(8), 3873-3882 (2015-03-18)
T cells develop functional defects during HIV-1 infection, partially due to the upregulation of inhibitory receptors such as programmed death-1 (PD-1) and CTLA-4. However, the role of lymphocyte activation gene-3 (LAG-3; CD223), also known as an inhibitory receptor, in HIV

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