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CLEC4D encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Additionally we are shipping CLEC4D Antibodies (77) and CLEC4D Kits (1) and many more products for this protein.
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Results show the molecular mechanism of glycolipid recognition through C-type lectin (show MBL2 Proteins) receptors, which may provide clues to rational design for effective adjuvants.
CLECSF8 functions as an activation receptor on myeloid cells and associates with a novel adaptor molecule
Cross-linking of the receptor leads to a rapid internalization suggesting that CLECSF8 constitutes and endocytic receptor.
MCL (macrophage C-type lectin) plays a crucial role in killing bacteria during Escherichia coli-induced peritonitis. MCL-deficient mice with E. coli-induced sepsis showed lower survival rates and reduced bacterial clearance when compared with control mice, despite similar levels of proinflammatory cytokine production.
activation of CLRs Dectin-2 (show CLEC6A Proteins) and Dectin-3 by fungi infections triggers them for ubiquitination and degradation in a Syk (show SYK Proteins)-dependent manner.
The authors report that microbial stimulation triggers Mincle (Clec4e (show CLEC4E Proteins)) expression through the myeloid differentiation primary response gene 88 (MyD88 (show MYD88 Proteins)) pathway; a process that does not require MCL (Clecsf8, Clec4d). Conversely, they show that MCL is constitutively expressed but retained intracellularly until Mincle (show CLEC4E Proteins) is induced, whereupon the receptors form heterodimers which are translocated to the cell surface.
Data show that Mincle (show CLEC4E Proteins), the inducible receptor for mycobacterial cord factor, is the key switch for the transition of macrophages from cytokine expression to high nitric oxide production.
MCL regulates the development of vaccine-induced Th17 cells and protective immunity against lethal experimental infection with Blastomyces dermatitidis.
major contributor to activation of innate immunity against M. bovis in experimental model, mirrors Mincle (show CLEC4E Proteins) expression
Clecsf8-/- mice exhibit higher bacterial burdens and increased mortality upon Mycobacterium tuberculosis infection.
These results suggest that MCL positively regulates Mincle (show CLEC4E Proteins) expression through protein-protein interaction via its stalk region, thereby magnifying Mincle (show CLEC4E Proteins)-mediated signaling.
Trehalose 6,6'-dimycolate-induced Mincle (show CLEC4E Proteins) expression is dependent on Dectin-3-mediated NF-kappaB (show NFKB1 Proteins) activation through the CARD9 (show CARD9 Proteins)-BCL10 (show BCL10 Proteins)-MALT1 (show MALT1 Proteins) complex.
Compared to their respective homodimers, Dectin-3 and Dectin-2 (show CLEC6A Proteins) heterodimers bound alpha-mannans more effectively, leading to potent inflammatory responses against fungal infections.
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. 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 D
, C-type lectin domain family 4 member D
, C-type (calcium dependent, carbohydrate-recognition domain) lectin, superfamily member 8
, C-type lectin receptor
, C-type lectin superfamily member 8
, C-type lectin-like receptor 6
, macrophage C-type lectin
, C-type (calcium dependent, carbohydrate recognition domain) lectin, superfamily member 8
, C-type lectin, superfamily member 8
, macrophage-restricted C-type lectin