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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 o. Additionally we are shipping C-Type Lectin Domain Family 1, Member B Antibodies (68) and C-Type Lectin Domain Family 1, Member B Proteins (10) and many more products for this protein.
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NZ-1 inhibits the hPDPN-CLEC-2 interaction and is also useful for anti-PA tag MAb.The minimum epitope of LpMab-13 was identified as Ala42-Asp49 of hPDPN using Western blot and flow cytometry. The combination of different epitope-possessing MAbs could be advantageous for the hPDPN-targeting diagnosis and therapy
CLEC2 prevents expression of PI3K (show PIK3CA ELISA Kits) subunits, in a SYK (show SYK ELISA Kits)-dependent manner, to suppress the invasive activities of gastric cancer cells.
CLEC-2 regulates Akt and MAPK downstream of PI3K and PKC, leading to phosphorylation and inhibition of GSK3alpha/beta, and enhanced platelet aggregation and secretion.
Data (including data from studies using recombinant proteins) suggest that a diverse range of ligands activate platelets through activation/phosphorylation (show CD36 ELISA Kits) of C (show GP6 ELISA Kits)D36/GPVI (glycoprotein VI) and/or CLEC-2 (C-type lectin-like receptor-2).
PI3K (show PIK3CA ELISA Kits) and Tec (show NR4A3 ELISA Kits) family kinases play a crucial role in the regulation of platelet activation and Syk (show SYK ELISA Kits) phosphorylation downstream of the CLEC-2 receptor
fucoidan is a novel CLEC-2 receptor agonist that activates platelets through a SFK-dependent signaling pathway
Dimerization of two phosphorylated CLEC-2 molecules leads to recruitment of the tyrosine kinase Syk via its tandem SH2 domains and initiation of a downstream signaling cascade
A differential proteomic analysis of basal and rhodocytin-activated platelets with the aim of providing novel clues on CLEC-2 signaling regulation.
The glycosylation sites (N120 and N134) are necessary for the surface expression of CLEC-2.
Shedding of CLEC-2 from the cell surface may reflect increased expression of this membrane protein and serve as a marker of disease activity.
A reciprocal interaction between CLEC-2 on megakaryocytes and PDPN (show PDPN ELISA Kits) on Bone marrow (BM) Fibroblastic reticular cell-like cells contributes to the periarteriolar megakaryopoietic microenvironment in mouse BM.
A role for CLEC2 as a regulator of macrophage polarity and Kupffer cell polarity, lipid and glucose homeostasis
Data indicate that C-type lectin-like receptor-2 (CLEC-2) is highly expressed on bone marrow megakaryocytes (Mks (show MKKS ELISA Kits)).
Data (including data from studies in transgenic mice) suggest that a diverse range of ligands activate platelets through activation/phosphorylation of Cd36 (show CD36 ELISA Kits)/GPVI (show GP6 ELISA Kits) (glycoprotein VI) and/or Clec-2 (C-type lectin-like receptor-2).
Podoplanin (show PDPN ELISA Kits) and CLEC-2 critically drive the formation and integrity of developing cerebral blood vessels.
PI3K and Tec (show NR4A3 ELISA Kits) family kinases play a crucial role in the regulation of platelet activation and Syk (show SYK ELISA Kits) phosphorylation downstream of the CLEC-2 receptor
CLEC-2 signaling promotes adhesion to Podoplanin (show PDPN ELISA Kits) and regulation of Podoplanin (show PDPN ELISA Kits) signaling, thereby contributing to lymphatic vasculature development.
Under resting conditions, when FRCs are unlikely to encounter mature DCs expressing the PDPN (show PDPN ELISA Kits) receptor CLEC-2, PDPN (show PDPN ELISA Kits) endowed FRCs with contractile function and exerted tension within the reticulum.
Functional studies of platelets from Ceacam2(-/-)-deficient mice (Cc2 (show TSG101 ELISA Kits)(-/-)) revealed that CEACAM2 serves to negatively regulate collagen glycoprotein VI (platelet) (GPVI (show GP6 ELISA Kits))-FcRgamma (show FCER1G ELISA Kits)-chain and the C-type lectinlike receptor 2 (CLEC-2) signaling
The results demonstrated that CLEC-2-dependent platelet activation is insensitive to cGMP-elevation and only partially sensitive to cAMP-elevation.
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
C-type lectin domain family 1, member B
, C-type lectin domain family 1 member B
, c-type lectin domain family 1 member B-like
, C-type lectin-like receptor 2
, C-type lectin-like receptor-2