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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

C-type lectin domain family 1, member B

CLEC-2, C-type lectin-like receptor 2
Natural killer (NK) cells express multiple calcium-dependent (C-type) lectin-like receptors, such as CD94 (KLRD1; MIM 602894) and NKG2D (KLRC4; MIM 602893), that interact with major histocompatibility complex class I molecules and either inhibit or activate cytotoxicity and cytokine secretion. CLEC2 is a C-type lectin-like receptor expressed in myeloid cells and NK cells (Colonna et al., 2000 [PubMed 10671229]).[supplied by OMIM, Jan 2011] (from NCBI)
Top mentioned proteins: CD45, Syk, GPVI, V1a, Src
Papers on CLEC-2
Establishment of Novel Monoclonal Antibody PMab-32 Against Rabbit Podoplanin.
Kato et al., Sendai, Japan. In Monoclon Antib Immunodiagn Immunother, Feb 2016
PDPN activates platelet aggregation by binding to C-type lectin-like receptor-2 (CLEC-2) on platelet.
Platelet immunoreceptor tyrosine-based activation motif (ITAM) and hemITAM signaling and vascular integrity in inflammation and development.
Bergmeier et al., Chapel Hill, United States. In J Thromb Haemost, Feb 2016
Murine platelets express two ITAM-containing receptors: the Fc receptor γ-chain (FcRγ), which functionally associates with the collagen receptor GPVI, and the C-type lectin-like 2 (CLEC-2) receptor, a hemITAM receptor for the mucin-type glycoprotein podoplanin.
Platelets Regulate the Migration of Keratinocytes via Podoplanin/CLEC-2 Signaling during Cutaneous Wound Healing in Mice.
Katoh et al., Kyoto, Japan. In Am J Pathol, Jan 2016
Podoplanin is an endogenous ligand for C-type lectin-like receptor 2 (CLEC-2), which is expressed on platelets.
Targeting a novel domain in podoplanin for inhibiting plateletmediated tumor metastasis.
Fujita et al., Tokyo, Japan. In Oncotarget, Jan 2016
PLAG4 has high homology to the previously reported PLAG3 and contributes to the binding of its platelet receptor CLEC-2.
Inflammation drives thrombosis after Salmonella infection via CLEC-2 on platelets.
Cunningham et al., In J Clin Invest, Jan 2016
Here, using a mouse model of systemic Salmonella Typhimurium infection, we determined that inflammation in tissues triggers thrombosis within vessels via ligation of C-type lectin-like receptor-2 (CLEC-2) on platelets by podoplanin exposed to the vasculature following breaching of the vessel wall.
Development of Sensitive Monoclonal Antibody PMab-2 Against Rat Podoplanin.
Kato et al., Sendai, Japan. In Monoclon Antib Immunodiagn Immunother, Dec 2015
Podoplanin (PDPN) is a platelet aggregation-inducing factor, which is known as an endogenous ligand of C-type lectin-like receptor-2 (CLEC-2).
Dextran sulfate triggers platelet aggregation via direct activation of PEAR1.
Hoylaerts et al., Leuven, Belgium. In Platelets, Dec 2015
UNASSIGNED: Dextran sulfate (DxS; Mr 500 kD) induces fibrinogen receptor (αIIbβ3) activation via CLEC-2/Syk signaling and via a Syk-independent SFK/PI3K/Akt-dependent tyrosine kinase pathway in human and murine platelets.
Emerging roles of podoplanin in vascular development and homeostasis.
Xia et al., Hangzhou, China. In Front Med, Nov 2015
PDPN on LECs or FRCs activates CLEC-2 in platelets, triggering platelet activation and/or aggregation through downstream signaling events, including activation of Syk kinase.
Sugar recognition and protein-protein interaction of mammalian lectins conferring diverse functions.
Yamaguchi et al., Wako, Japan. In Curr Opin Struct Biol, Oct 2015
Simultaneous recognition of both glycan and the aglycon moieties enhances the affinity and specificity of lectins such as CLEC-2 and PILRα.
Impact of the PI3-kinase/Akt pathway on ITAM and hemITAM receptors: haemostasis, platelet activation and antithrombotic therapy.
Watson et al., Birmingham, United Kingdom. In Biochem Pharmacol, May 2015
Platelets also express another receptor, C-type lectin 2 (CLEC-2), which has a single YxxL sequence, so it is appropriately called a hemITAM receptor.
The CLEC-2-podoplanin axis controls the contractility of fibroblastic reticular cells and lymph node microarchitecture.
Turley et al., Boston, United States. In Nat Immunol, 2015
Under resting conditions, when FRCs are unlikely to encounter mature DCs expressing the PDPN receptor CLEC-2, PDPN endowed FRCs with contractile function and exerted tension within the reticulum.
Targeting platelet receptors in thrombotic and thrombo-inflammatory disorders.
Nieswandt et al., Würzburg, Germany. In Hamostaseologie, 2014
This review summarizes recent developments in understanding the function of glycoprotein (GP)Ib, GPVI and the C-type lectin-like receptor 2 (CLEC-2) in hemostasis, arterial thrombosis and thrombo-inflammation and will discuss the suitability of the receptors as novel targets to treat these diseases in humans.
Dendritic cells control fibroblastic reticular network tension and lymph node expansion.
Reis e Sousa et al., London, United Kingdom. In Nature, 2014
Here we report that the physical elasticity of lymph nodes is maintained in part by podoplanin (PDPN) signalling in stromal fibroblastic reticular cells (FRCs) and its modulation by CLEC-2 expressed on dendritic cells.
Podoplanin maintains high endothelial venule integrity by interacting with platelet CLEC-2.
Xia et al., Oklahoma City, United States. In Nature, 2013
Further analyses demonstrated that PDPN expressed on fibroblastic reticular cells, which surround HEVs, functions as an activating ligand for platelet C-type lectin-like receptor 2 (CLEC-2, also known as CLEC1B).
Podoplanin-rich stromal networks induce dendritic cell motility via activation of the C-type lectin receptor CLEC-2.
Turley et al., Boston, United States. In Immunity, 2012
activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in dendritic cells to promote efficient motility along stromal surfaces.
Platelet activation receptor CLEC-2 regulates blood/lymphatic vessel separation by inhibiting proliferation, migration, and tube formation of lymphatic endothelial cells.
Ozaki et al., Japan. In J Biol Chem, 2012
platelets regulate blood/lymphatic vessel separation by inhibiting the proliferation, migration, and tube formation of LECs, mainly because of the release of BMP-9 upon activation by CLEC-2/podoplanin in
Platelet CLEC-2 and podoplanin in cancer metastasis.
Watson et al., Birmingham, United Kingdom. In Thromb Res, 2012
Here, the bidirectional relationship between CLEC-2 and podoplanin is described and considered in the context of tumour growth and metastasis.
CLEC-2 and Syk in the megakaryocytic/platelet lineage are essential for development.
Watson et al., Birmingham, United Kingdom. In Blood, 2012
Megakaryocyte/platelet expression of CLEC-2 and Syk is required for normal brain vasculature and lymphatic development and platelet CLEC-2 and Syk directly modulate lymphatic endothelial cell behavior in vitro.
CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses.
Reis e Sousa et al., London, United Kingdom. In Eur J Immunol, 2011
CLEC-2 is expressed in myeloid cells and acts as a Syk-coupled C-type lectin receptor able to modulate TLR signaling and inflammatory responses
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