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CLEC4D encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Zusätzlich bieten wir Ihnen CLEC4D Antikörper (71) und CLEC4D Proteine (10) und viele weitere Produktgruppen zu diesem Protein an.
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Results show the molecular mechanism of glycolipid recognition through C-type lectin 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.
Dectin-3 deficiency did not lead to increased susceptibility of mice to experimental pulmonary C. neoformans infection. Also, no significant differences in pulmonary leukocyte recruitment and cytokine production were observed in Dectin-3 deficient mice compared to wild type infected mice
activation of CLRs Dectin-2 and Dectin-3 by fungi infections triggers them for ubiquitination and degradation in a Syk-dependent manner.
The authors report that microbial stimulation triggers Mincle (Clec4e) expression through the myeloid differentiation primary response gene 88 (MyD88) pathway; a process that does not require MCL (Clecsf8, Clec4d). Conversely, they show that MCL is constitutively expressed but retained intracellularly until Mincle is induced, whereupon the receptors form heterodimers which are translocated to the cell surface.
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.
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 expression
Clecsf8-/- mice exhibit higher bacterial burdens and increased mortality upon Mycobacterium tuberculosis infection.
These results suggest that MCL positively regulates Mincle expression through protein-protein interaction via its stalk region, thereby magnifying Mincle-mediated signaling.
Trehalose 6,6'-dimycolate-induced Mincle expression is dependent on Dectin-3-mediated NF-kappaB activation through the CARD9-BCL10-MALT1 complex.
Compared to their respective homodimers, Dectin-3 and Dectin-2 heterodimers bound alpha-mannans more effectively, leading to potent inflammatory responses against fungal infections.
Clec4d(-/-) neutrophils did not exhibit any defect in bacterial clearance
These results suggest that Clec4d is an FcRgamma-coupled activating receptor that mediates the adjuvanticity of trehalose-6,6'-dimycolate.
The genomic organization of the MCL gene and the sequence of the promoter region were determined
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