Recombinant Human CLEC4E Fc Chimera Protein, CF Summary
Details of Functionality
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 Human CLEC4E Fc Chimera that produces 50% of the optimal binding response is approximately 0.05-0.3 μg/mL.
Source
Chinese Hamster Ovary cell line, CHO-derived human CLEC4E protein
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity
Theoretical MW
47 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
54-64 kDa, reducing conditions
Publications
Read Publication using 8995-CL in the following applications:
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). Human CLEC4E consists of a 19 amino acid (aa) cytoplasmic domain, a 21 aa transmembrane segment, and a 179 aa extracellular domain (ECD) that contains the C-type lectin domain (2). Within the ECD, human CLEC4E shares 65% and 68% aa sequence identity with mouse 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).
Richardson, M.B. and S.J. Williams (2014) Front. Immunol. 5:288.
Matsumoto, M. et al. (1999) J. Immunol. 163:5039.
Ishikawa, E. et al. (2009) J. Exp. Med. 206:2879.
Wells, C.A. et al. (2008) J. Immunol. 180:7404.
Yamasaki, S. et al. (2008) Nat. Immunol. 9:1179.
Lobato-Pascual, A. et al. (2013) Eur. J. Immunol. 43:3167.
Hattori, Y. et al. (2014) J. Biol. Chem. 289:15405.
Ostrop, J. et al. (2015) J. Immunol. 195:2417.
Wevers, B.A. et al. (2014) Cell Host Microbe 15:494.
Ishikawa, T. et al. (2013) Cell Host Microbe 13:477.
Kiyotake, R. et al. (2015) J. Biol. Chem. 290:25322.
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