• Purity

  >90%, 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.  

• Activity

  Measured by its binding ability in a functional ELISA. When Trehalose 6, 6'-Dimycolate is immobilized at 1 µg/mL (100 µL/well), the concentration of Recombinant Mouse CLEC4E Fc Chimera that produces 50% of the optimal binding response is approximately 8-48 ng/mL.

• Source

  Chinese Hamster Ovary cell line, CHO-derived

  MDP	Mouse IgG2A (Glu98-Lys330)	IEGR	Mouse CLEC4E (Thr46-Asp214) Accession # Q9R0Q8
  N-terminus			C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  Met

• Structure / Form

  Disulfide-linked homodimer

• Predicted Molecular Mass

  47 kDa

• SDS-PAGE

  54-63 kDa, reducing conditions

Data Images

Background: CLEC4E

CLEC4E, also known as Mincle, is an approximately 30 kDa type 2 transmembrane C-type lectin that functions as an activating innate immune receptor (1). Mouse CLEC4E consists of a 19 amino acid (aa) cytoplasmic domain, a 21 aa transmembrane segment, and a 174 aa extracellular domain (ECD) that contains the C-type lectin domain (2). Within the ECD, mouse CLEC4E shares 65% and 87% aa sequence identity with human and rat CLEC4E, respectively. CLEC4E is expressed on monocytes, macrophages, and immature dendritic cells (2-5). It associates with CLEC4D/MCL and the gamma chain signaling subunits of Fc receptors (mediated by an Arg residue in the CLEC4E transmembrane segment) (3, 5, 6). Human CLEC4E binds to mycobacterial glycolipids including the immune adjuvant TDM (cord factor), its synthetic analog TDB, and GroMM (3, 4, 7-10). It also binds the nuclear protein SAP130 which can be released from necrotic cells (5) and cholesterol crystals deposited in atherosclerotic plaques (11). Mouse CLEC4E, in contrast, does not appear to interact with TDB, GroMM, or cholesterol crystals (7, 8, 11). CLEC4E ligation triggers phagocytosis and the production of inflammatory chemokines and cytokines (3-6, 8, 10). The fungus Fonsecaea monophora may evade immune clearance through binding to CLEC4E and suppressing IL-12 production and Th1 cell differentiation instead of promoting inflammation (9).

• References:

1. Richardson, M.B. and S.J. Williams (2014) Front. Immunol. 5:288.

2. Matsumoto, M. et al. (1999) J. Immunol. 163:5039.

3. Ishikawa, E. et al. (2009) J. Exp. Med. 206:2879.

4. Wells, C.A. et al. (2008) J. Immunol. 180:7404.

5. Yamasaki, S. et al. (2008) Nat. Immunol. 9:1179.

6. Lobato-Pascual, A. et al. (2013) Eur. J. Immunol. 43:3167.

7. Hattori, Y. et al. (2014) J. Biol. Chem. 289:15405.

8. Ostrop, J. et al. (2015) J. Immunol. 195:2417.

9. Wevers, B.A. et al. (2014) Cell Host Microbe 15:494.

10. Ishikawa, T. et al. (2013) Cell Host Microbe 13:477.

11. Kiyotake, R. et al. (2015) J. Biol. Chem. 290:25322.

• Long Name:

  C-type Lectin Domain Family 4, Member E

• Entrez Gene IDs:

  26253 (Human); 56619 (Mouse); 450223 (Rat)

• Alternate Names:

  CLEC4E; CLECSF9; C-type (calcium dependent, carbohydrate-recognition domain) lectin, superfamilymember 9; C-type lectin domain family 4 member E; C-type lectin domain family 4, member E; Macrophage-inducible C-type lectin; MINCLE; MINCLEC-type lectin superfamily member 9