Human CLEC4E Antibody Summary
Arg41-Leu219
Accession # Q9ULY5
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
Detection of CLEC4e in HEK293 Human Cell Line Transfected with Human CLEC4e and eGFP by Flow Cytometry. HEK293 human embryonic kidney cell line transfected with either (A) human CLEC4e or (B) irrelevant protein and eGFP was stained with Rabbit Anti-Human CLEC4e Monoclonal Antibody (Catalog # MAB8995) followed by Allophycocyanin-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # F0111). Quadrant markers were set based on control antibody staining (Catalog # MAB1050). View our protocol for Staining Membrane-associated Proteins.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
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). 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.
Product Datasheets
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