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CLEC4D encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. 再加上，我们可以发CLEC4D 蛋白 (10) 和 CLEC4D 试剂盒 (1)和数多这个蛋白质的别的产品。
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Human Monoclonal CLEC4D Primary Antibody for FACS - ABIN4897646
Graham, Gupta, Schafer, Reid, Kimberg, Dennehy, Hornsell, Guler, Campanero-Rhodes, Palma, Feizi, Kim, Sobieszczuk, Willment, Brown: The C-type lectin receptor CLECSF8 (CLEC4D) is expressed by myeloid cells and triggers cellular activation through Syk kinase. in The Journal of biological chemistry 2012
Results show the molecular mechanism of glycolipid recognition through C-type lectin (显示 MBL2 抗体) 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 (显示 CLEC6A 抗体) and Dectin-3 by fungi infections triggers them for ubiquitination and degradation in a Syk (显示 SYK 抗体)-dependent manner.
The authors report that microbial stimulation triggers Mincle (Clec4e (显示 CLEC4E 抗体)) expression through the myeloid differentiation primary response gene 88 (MyD88 (显示 MYD88 抗体)) pathway; a process that does not require MCL (Clecsf8, Clec4d). Conversely, they show that MCL is constitutively expressed but retained intracellularly until Mincle (显示 CLEC4E 抗体) is induced, whereupon the receptors form heterodimers which are translocated to the cell surface.
Data show that Mincle (显示 CLEC4E 抗体), 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 (显示 CLEC4E 抗体) expression
Clecsf8-/- mice exhibit higher bacterial burdens and increased mortality upon Mycobacterium tuberculosis infection.
These results suggest that MCL positively regulates Mincle (显示 CLEC4E 抗体) expression through protein-protein interaction via its stalk region, thereby magnifying Mincle (显示 CLEC4E 抗体)-mediated signaling.
Trehalose 6,6'-dimycolate-induced Mincle (显示 CLEC4E 抗体) expression is dependent on Dectin-3-mediated NF-kappaB (显示 NFKB1 抗体) activation through the CARD9 (显示 CARD9 抗体)-BCL10 (显示 BCL10 抗体)-MALT1 (显示 MALT1 抗体) complex.
Compared to their respective homodimers, Dectin-3 and Dectin-2 (显示 CLEC6A 抗体) 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