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CLEC4E encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Additionally we are shipping CLEC4E Kits (14) and CLEC4E Proteins (10) and many more products for this protein.
Showing 10 out of 63 products:
Human Monoclonal CLEC4E Primary Antibody for EIA, IF - ABIN487350
Ishikawa, Ishikawa, Morita, Toyonaga, Yamada, Takeuchi, Kinoshita, Akira, Yoshikai, Yamasaki: Direct recognition of the mycobacterial glycolipid, trehalose dimycolate, by C-type lectin Mincle. in The Journal of experimental medicine 2009
Show all 3 references for ABIN487350
Human Monoclonal CLEC4E Primary Antibody for ELISA, WB - ABIN565251
Bugarcic, Hitchens, Beckhouse, Wells, Ashman, Blanchard: Human and mouse macrophage-inducible C-type lectin (Mincle) bind Candida albicans. in Glycobiology 2008
Show all 2 references for ABIN565251
Human Monoclonal CLEC4E Primary Antibody for ELISA, ICC - ABIN4299166
de Rivero Vaccari, Brand, Berti, Alonso, Bullock, de Rivero Vaccari: Mincle signaling in the innate immune response after traumatic brain injury. in Journal of neurotrauma 2015
CLEC4E expression is significantly upregulated in human masticatory mucosa during wound healing
The expression of Mincle increases significantly during the early period of Aspergillus fumigatus infection, while expression of eight corresponding cytokines changes. Mincle, as a pattern recognition receptor, may play a role in the early innate immune response of the corneal resistance against fungus.
Induction of Mincle by Helicobacter pylori and consequent anti-inflammatory signaling denote a bacterial survival strategy.
our findings identify mincle as a contributor to the inflammatory response after traumatic brain injury
Data indicate that MINCLE receptor is able to mediate the response to trehalose-6,6-dimycolate (TDM) dependent on SYK (show SYK Antibodies) kinase and CARD9 (show CARD9 Antibodies) protein.
mincle is a fungal receptor that can suppress antifungal immunity and, as such, is a potential therapeutic target.
These results demonstrated that GroMM is a unique ligand for human Mincle that is not recognized by mouse Mincle.
Results show the molecular mechanism of glycolipid recognition through C-type lectin (show MBL2 Antibodies) receptors, which may provide clues to rational design for effective adjuvants.
Macrophage-inducible C-type lectin is associated with anti-cyclic citrullinated peptide antibodies-positive rheumatoid arthritis in men.
Mincle is a potentially critical player in human B cell responses.
this paper shows that mycobacterial cell envelope glycolipid TDM modulates TLR2 (show TLR2 Antibodies)-mediated IL-10 (show IL10 Antibodies) and IL-12p40 responses in macrophages through Mincle, which is, in turn, up-regulated by Mycobacterium bovis BCG (show SLC11A1 Antibodies)
Data show that Mincle, the inducible receptor for mycobacterial cord factor, is the key switch for the transition of macrophages from cytokine expression to high nitric oxide production.
Mincle Activation and the Syk (show SYK Antibodies)/Card9 (show CARD9 Antibodies) Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye
work shows parallel networks of necroptosis-induced CXCL1 (show CXCL1 Antibodies) and Mincle signalling that promote macrophage-induced adaptive immune suppression and thereby enable pancreatic ductal adenocarcinoma progression
The results indicate differential roles for Dectin-2 (show CLEC6A Antibodies) and Mincle in the generation of adaptive immune responses to F. pedrosoi fungal infection in mice.
Mincle is essential for the activation of macrophages by trehalose glycolipids, the receptor does not play a role in the uptake of these glycolipids or of glycolipid-coated particles.
These results suggest that MCL (show CLEC4D Antibodies) positively regulates Mincle expression through protein-protein interaction via its stalk region, thereby magnifying Mincle-mediated signaling.
Collectively, authors show that expression of Mincle, particularly by classical dendritic cells, contributes to the control of splenic Mycobacterium bovis BCG (show SLC11A1 Antibodies) infection in mice.
Trehalose 6,6'-dimycolate-induced Mincle expression is dependent on Dectin-3-mediated NF-kappaB (show NFKB1 Antibodies) activation through the CARD9 (show CARD9 Antibodies)-BCL10 (show BCL10 Antibodies)-MALT1 (show MALT1 Antibodies) complex.
identify C/EBPbeta as central hub in Mincle expression and inflammatory gene induction, whereas HIF1alpha controls Nos2 expression.
The data demonstrate how mincle bridges between the surfaces of the macrophage and the mycobacterium.
the function of the guinea pig homologue of Mincle (gpMincle) and MCL (show CLEC4D Antibodies) (gpMCL). gpMincle directly bound to trehalose-6,6'-dimycolate
This gene encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Members of this family share a common protein fold and have diverse functions, such as cell adhesion, cell-cell signalling, glycoprotein turnover, and roles in inflammation and immune response. The encoded type II transmembrane protein is a downstream target of CCAAT/enhancer binding protein (C/EBP), beta (CEBPB) and may play a role in inflammation. Alternative splice variants have been described but their full-length sequence has not been determined. This gene is closely linked to other CTL/CTLD superfamily members on chromosome 12p13 in the natural killer gene complex region.
C-type lectin domain family 4, member E
, C-type (calcium dependent, carbohydrate-recognition domain) lectin, superfamily member 9
, C-type lectin domain family 4 member E
, C-type lectin superfamily member 9
, macrophage-inducible C-type lectin
, C-type (calcium dependent, carbohydrate recognition domain) lectin, superfamily member 9
, C-type lectin, superfamily member 9