Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
CLEC4E encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Zusätzlich bieten wir Ihnen CLEC4E Antikörper (61) und CLEC4E Kits (16) und viele weitere Produktgruppen zu diesem Protein an.
Showing 8 out of 11 products:
Human CLEC4E Protein expressed in HEK-293 Cells - ABIN2712869
Wevers, Kaptein, Zijlstra-Willems, Theelen, Boekhout, Geijtenbeek, Gringhuis: Fungal engagement of the C-type lectin mincle suppresses dectin-1-induced antifungal immunity. in Cell host & microbe 2014
combination adjuvant systems demonstrate markedly different immune activation with age, with combined DC activation via Macrophage-inducible C-type lectin and TLR7 (zeige TLR7 Proteine)/8 representing a novel approach to enhance the efficacy of early-life vaccines.
We here show that Mincle gene expression was induced in alveolar macrophages and neutrophils in bronchoalveolar lavage fluids of mice and patients with pneumococcal pneumonia
a nonredundant role for Clec4e in coordinating major biological pathways involved in atherosclerosis
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 (zeige SYK Proteine) kinase and CARD9 (zeige CARD9 Proteine) 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.
Mincle is induced specifically on M1 macrophages, where Mincle-Syk (zeige SYK Proteine) signaling promotes and maintains inflammatory phenotypes of M1 macrophages in acute renal inflammation.
work implicates a novel innate immune driver of Con (zeige KITLG Proteine) A hepatitis and, more broadly, suggests a potential role for Mincle in diseases governed by sterile inflammation.
Mincle deletion results in TLR4 (zeige TLR4 Proteine)-mediated inflammation.
Priming by Mincle-deficient dendritic cells (DCs).
Thus, macrophage activation by the corynebacterial cell wall relies on TLR2-driven robust Mincle expression and the cooperative action of both receptors.
this study shows that immune activation in vitro and in vivo by trehalose esters of simple fatty acids requires two acyl chains of length and involves Mincle
Attenuated neutrophil extracellular trap formation in Mincle-/- neutrophils correlates with impaired autophagy activation in vitro and in vivo, whereas reactive oxygen species formation in these neutrophils remained intact.
this study shows a significant role for Mincle in Pneumocystis modulating host defense during infection
The authors report that microbial stimulation triggers Mincle (Clec4e) expression through the myeloid differentiation primary response gene 88 (MyD88 (zeige MYD88 Proteine)) pathway; a process that does not require MCL (Clecsf8 (zeige CLEC4D Proteine), Clec4d (zeige CLEC4D Proteine)). Conversely, they show that MCL (zeige CLEC4D Proteine) is constitutively expressed but retained intracellularly until Mincle is induced, whereupon the receptors form heterodimers which are translocated to the cell surface.
The structure of an extended portion of the extracellular domain of mincle, beyond the minimal C-type carbohydrate recognition domain, also constrains the way the binding domains may interact on the surface of macrophages.
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 (zeige CLEC4D Proteine) (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