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C-type lectin domain family 4, member E

Mincle, Macrophage-inducible C-type lectin, Clecsf9, C-type lectin superfamily member 9, Clec4e
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Syk, CARD9, Dectin-2, Dectin-1, CAN
Papers on Mincle
Immune sensing of microbial glycolipids and related conjugates by T cells and the pattern recognition receptors MCL and Mincle.
Review
New
Williams et al., Melbourne, Australia. In Carbohydr Res, Feb 2016
The pattern recognition receptors macrophage C-type lectin (MCL) and macrophage inducible C-type lectin (Mincle) receptors sense glycolipids and through signalling initiate cellular activation, shaping immune responses to peptide antigens, including the differentiation of naïve T cells into conventional effector T helper cells.
Mincle suppresses Toll-like receptor 4 activation.
New
Miller et al., New York City, United States. In J Leukoc Biol, Feb 2016
We found that Mincle, a C-type lectin receptor, regulates proinflammatory Toll-like receptor 4 signaling.
The mycobacterial receptor, Clec4d (CLECSF8, MCL) is co-regulated with Mincle and upregulated on mouse myeloid cells following microbial challenge.
New
Brown et al., Aberdeen, United Kingdom. In Eur J Immunol, Dec 2015
UNASSIGNED: The C-type lectin receptor (CTLR), Clec4d (MCL, CLECSF8), is a member of the Dectin-2 cluster of CTLRs, which also includes the related receptors Mincle and Dectin-2.
Phenotypic and Functional Characterization of Monoclonal Antibodies with Specificity for Rhesus Macaque CD200, CD200R and Mincle.
Ansari et al., Atlanta, United States. In Plos One, 2014
In efforts to gain further insight on the potential role of these lectin-like molecules, our laboratory generated monoclonal antibodies (mAb) against the human analogs of rhesus macaque CD200, CD200R and Mincle, since the rhesus macaques are accepted as the most reliable animal model to study human HIV infection.
Induction of Mincle by Helicobacter pylori and consequent anti-inflammatory signaling denote a bacterial survival strategy.
Ahmed et al., Hyderābād, India. In Sci Rep, 2014
The recognition of glyco or carbohydrate moieties by Mincle (Macrophage inducible C-type lectin) is emerging as a crucial element in anti-fungal and anti-mycobacterial immunity.
AAL exacerbates pro-inflammatory response in macrophages by regulating Mincle/Syk/Card9 signaling along with the Nlrp3 inflammasome assembly.
Wang et al., Wuhan, China. In Am J Transl Res, 2014
Mechanistic studies revealed that AAL likely targets macrophages through receptor Mincle to activate Syk/Card9 signaling, which then couples to the Nlrp3 inflammasome assembly.
Mincle, an Innate Immune Receptor, Is Expressed in Urothelial Cancer Cells of Papillomavirus-Associated Urothelial Tumors of Cattle.
Roperto et al., Napoli, Italy. In Plos One, 2014
BACKGROUND: Mincle, macrophage-inducible C-type lectin, is a member of C-type lectin receptors.
MCL and Mincle: C-Type Lectin Receptors That Sense Damaged Self and Pathogen-Associated Molecular Patterns.
Review
Williams et al., Melbourne, Australia. In Front Immunol, 2013
Macrophage C-type lectin (MCL) and macrophage inducible C-type lectin (Mincle) comprise part of an extensive repertoire of pattern recognition receptors with the ability to sense damage-associated and pathogen-associated molecular patterns.
C-type lectin MCL is an FcRγ-coupled receptor that mediates the adjuvanticity of mycobacterial cord factor.
Impact
Yamasaki et al., Fukuoka, Japan. In Immunity, 2013
We herein report that the C-type lectin MCL (also called Clec4d) is a TDM receptor that is likely to arise from gene duplication of Mincle (also called Clec4e).
The Dectin-2 family of C-type lectin-like receptors: an update.
Review
Brown et al., Aberdeen, United Kingdom. In Int Immunol, 2013
Of relevance here is the dendritic cell-associated C-type lectin-2 (Dectin-2) family of CTLRs, which includes blood dendritic cell antigen 2 (BDCA-2), dendritic cell immunoactivating receptor (DCAR), dendritic cell immunoreceptor (DCIR), Dectin-2, C-type lectin superfamily 8 (CLECSF8) and macrophage-inducible C-type lectin (Mincle).
C-type lectin receptor-induced NF-κB activation in innate immune and inflammatory responses.
Review
Lin et al., Houston, United States. In Cell Mol Immunol, 2012
Recent studies indicate that many CLRs, such as Dectin-1, Dectin-2 and Mincle, function as pattern recognition receptors (PRRs) recognizing carbohydrate ligands from infected microorganisms.
Syk kinase-coupled C-type lectin receptors engage protein kinase C-σ to elicit Card9 adaptor-mediated innate immunity.
Impact
Ruland et al., München, Germany. In Immunity, 2012
Prkcd(-/-) dendritic cells, but not those lacking PKCα, PKCβ, or PKCθ, were defective in innate responses to Dectin-1, Dectin-2, or Mincle stimulation.
Silencing of renal DNaseI in murine lupus nephritis imposes exposure of large chromatin fragments and activation of Toll like receptors and the Clec4e.
GeneRIF
Mortensen et al., Tromsø, Norway. In Plos One, 2011
silencing of renal DNaseI gene expression initiates a cascade of inflammatory signals including activation of Toll like receptors and Clec4e, leading to progression of both murine and human lupus nephritis
Neutrophils Promote Mycobacterial Trehalose Dimycolate-Induced Lung Inflammation via the Mincle Pathway.
GeneRIF
Kim et al., Seoul, South Korea. In Plos Pathog, 2011
The physiological relevance of the Mincle-mediated anti-TDM immune response was confirmed by defective immune responses in Mincle/ mice upon aerosol infections with Mtb.
The biology of Mycobacterium cord factor and roles in pathogen-host interaction.
Review
Xie et al., Beibei, China. In Crit Rev Eukaryot Gene Expr, 2011
This progress is summarized in this paper, especially the receptors of cord factor, such as Toll-like receptors and Mincle.
Increased expression of macrophage-inducible C-type lectin in adipose tissue of obese mice and humans.
GeneRIF
Ogawa et al., Tokyo, Japan. In Diabetes, 2011
Our data suggest that Mincle is induced in adipose tissue macrophages in obesity at least partly through the saturated fatty acid/TLR4/NF-kappaB pathway, thereby suggesting its pathophysiologic role in obesity-induced adipose tissue inflammation.
Mast cells generated from patients with atopic eczema have enhanced levels of granule mediators and an impaired Dectin-1 expression.
GeneRIF
Scheynius et al., Stockholm, Sweden. In Allergy, 2011
progenitor-derived mast cells expressed the macrophage-inducible C-type lectin receptor Mincle, and exposure of these cells to M. sympodialis induced up-regulation of the mRNA expression of Mincle
Cutting edge: Mincle is essential for recognition and adjuvanticity of the mycobacterial cord factor and its synthetic analog trehalose-dibehenate.
GeneRIF
Lang et al., Erlangen, Germany. In J Immunol, 2010
Mincle is a key C-type lectin receptor for mycobacterial cord factor and controls T helper cell type (Th)1/Th cell type (Th)17 adjuvanticity of cord factor trehalose-6,6-dimycolate (TDM) and trehalose-6,6-dibehenate (TDB).
Sensing necrosis with Mincle.
Review
Impact
Brown, Cape Town, South Africa. In Nat Immunol, 2008
New data show that the C-type lectin Mincle is involved in this process.
Mincle is an ITAM-coupled activating receptor that senses damaged cells.
Impact
GeneRIF
Saito et al., Yokohama, Japan. In Nat Immunol, 2008
Mincle is a receptor that senses nonhomeostatic cell death and thereby induces the production of inflammatory cytokines to drive the infiltration of neutrophils into damaged tissue.
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