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Recombinant Mouse LSECtin/CLEC4G Protein, CF

Catalog # 10363-CL | R&D Systems, Inc. a Bio-Techne Brand
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10363-CL-050

Key Product Details

Source

CHO

Accession #

Conjugate

Unconjugated

Applications

Bioactivity

Product Specifications

Source

Chinese Hamster Ovary cell line, CHO-derived mouse LSECtin/CLEC4G protein

Hemagglutinin Tag
(YPYDVPDYA)

Mouse LSECtin/CLEC4G
(Leu52-Tyr294)
Accession # Q8BNX1
N-terminus C-terminus

Purity

>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.

Endotoxin Level

<0.10 EU per 1 μg of the protein by the LAL method.

N-terminal Sequence Analysis

Tyr

Predicted Molecular Mass

29 kDa

SDS-PAGE

36-44 kDa, under reducing conditions

Activity

Measured by its binding ability in a functional ELISA.
When Recombinant Mouse BTNL4 Fc Chimera (Catalog # 9590-BT) is immobilized at 2 µg/mL (100 µL/well), Recombinant Mouse LSECtin/CLEC4G (Catalog # 10363-CL) binds with an ED50 of 0.15-1.2 μg/mL.

Scientific Data Images for Recombinant Mouse LSECtin/CLEC4G Protein, CF

Recombinant Mouse LSECtin/CLEC4G Protein Binding Activity

Recombinant Mouse LSECtin/CLEC4G Protein Binding Activity

When Recombinant Mouse BTNL4 Fc Chimera (Catalog # 9590-BT) is immobilized at 2 µg/mL (100 µg/well), Recombinant Mouse LSECtin/CLEC4G (Catalog # 10363-CL) binds with an ED50 of 0.15-1.2 µg/mL.
Recombinant Mouse LSECtin/CLEC4G Protein SDS-PAGE

Recombinant Mouse LSECtin/CLEC4G Protein SDS-PAGE

2 μg/lane of Recombinant Mouse LSECtin/CLEC4G (Catalog # 10363-CL) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at 36-44 kDa and 110-130 kDa, repsectively.

Formulation, Preparation and Storage

10363-CL
Formulation Lyophilized from a 0.2 μm filtered solution in PBS.
Reconstitution Reconstitute at 500 μg/mL in PBS.
Shipping The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.

Background: LSECtin/CLEC4G

LSECtin (liver and lymph node sinusoidal endothelial cell C-type lectin), also known as C-type lectin superfamily 4 member G (CLEC4G), is a member of subgroup II of the C-type (Ca2+-dependent) lectin superfamily (1). The protein was named LSECtin because its initial expression was described to be restricted to liver and lymph node sinusoidal endothelial cells (1). However, LSECtin has also been detected in peripheral blood and thymic dendritic cells isolated ex vivo, and in monocyte-derived macrophages and dendritic cells at the RNA and protein level (2). Mouse LSECtin is a type II transmembrane glycoprotein that includes an N-terminal cytoplasmic tail (aa 1-30), a 21 aa transmembrane region, and a 243 aa extracellular domain (ECD). Within the ECD, mouse LSECtin shares 66% and 85% aa sequence identity with human and rat LSECtin, respectively. LSECtin binds to mannose, GlcNAc, and fucose in a Ca2+-dependent manner (1-3). In addition, LSECtin has the ability to bind to surface glycoproteins of enveloped viruses (3, 4). In particular, interaction of LSECtin with the surface glycoproteins of severe acute respiratory syndrome (SARS) coronavirus and Ebola virus has been described, and LSECtin-mediated infection of cells by Ebola virus has been demonstrated (3, 4). LSECtin is highly expressed on tumor-associated macrophages (TAMs) and enhances stemness of breast cancer cells (BCCs) (9). We identified BTN3A3, a B7 family member with previously unknown functions as the receptor for LSECtin on BCCs responsible for stemness-promoting effect of LSECtin (9). In mice bearing human tumor xenografts, either macrophage-specific ablation of LSECtin or silencing of BTN3A3 in BCCs decreased CSC frequency and tumor growth (9). Administration of LSECtin-positive macrophages increased the tumorigenic activity of BCCs dependent on BTN3A3 (9). Disruption of the LSECtin-BTN3A3 axis with BTN3A3-Fc or anti-BTN3A3 mAb has a therapeutic effect on breast cancer (9). These findings define a juxtacrine signaling mechanism by which TAMs promote cancer stemness (9). Targeting this axis in the CSC niche may provide potential therapies to breast cancer (9).

References

  1. Liu, W. et al. (2004) J. Biol. Chem. 279:18748.
  2. Dominguez-Soto, A. et al. (2007) Blood 109:5337.
  3. Powlesland, A. et al. (2008) J. Biol. Chem. 283:593.
  4. Gramberg, T. et al. (2005) Virology 340:224.
  5. Yamashiro, H. et al. (2010) J. Leukoc Biol. 88:757.
  6. Compte, E. et al. (2004) Eur. J. Immunol. 34:2089.
  7. Abeler-Dorner, L. et al. (2012) Trends Immunol. 33:34.
  8. Bas, A. et al. (2011) Proc Natl Acad Sci U S A. 108:4376.
  9. Liu, D. et al. (2019) Cell Res. 29:5.

Long Name

Liver And Lymph Node Sinusoidal Endothelial Cell C-type Lectin

Alternate Names

CLEC4G, Q6UXB4

Entrez Gene IDs

339390 (Human); 75863 (Mouse)

Gene Symbol

CLEC4G

UniProt

Product Documents for Recombinant Mouse LSECtin/CLEC4G Protein, CF

Certificate of Analysis

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Note: Certificate of Analysis not available for kit components.

Product Specific Notices for Recombinant Mouse LSECtin/CLEC4G Protein, CF

For research use only

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