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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 or activate cytotoxicity and cytokine secretion. 再加上，我们可以发C-Type Lectin Domain Family 1, Member B 抗体 (124) 和 C-Type Lectin Domain Family 1, Member B 试剂盒 (1)和数多这个蛋白质的别的产品。
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the CHIP/CLEC-2 axis may play an important role in the modulation of immune response.
Data (including data from studies using cells from knockout mice) suggest that CLEC2/CLEC2R signaling is dependent on thromboxane A2 generation and is potentiated by co-stimulation with different GNAQ (显示 GNAQ 蛋白) agonists. (CLEC2 = C-type lectin (显示 MBL2 蛋白) CLEC2; CLEC2R = CLEC2 receptor; GNAQ (显示 GNAQ 蛋白) = guanine nucleotide-binding protein (显示 COASY 蛋白) G[q] subunit alpha)
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 (显示 PIK3CA 蛋白) subunits, in a SYK (显示 SYK 蛋白)-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 (显示 CD36 蛋白) of C (显示 GP6 蛋白)D36/GPVI (glycoprotein VI) and/or CLEC-2 (C-type lectin-like receptor-2).
PI3K (显示 PIK3CA 蛋白) and Tec (显示 NR4A3 蛋白) family kinases play a crucial role in the regulation of platelet activation and Syk (显示 SYK 蛋白) 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.
CLEC-2 deficiency may inhibit thrombus formation in tumor vessels and increase the density of functional vessels, thus improving oxygen and nutrient supply to tumors, indirectly promoting tumor proliferation
these data suggest that the platelet CLEC-2-podoplanin (显示 PDPN 蛋白) signaling axis regulates the severity of lung inflammation in mice and is a possible novel target for therapeutic intervention in patients at risk of developing ARDS.
a hemITAM signaling-independent role for CLEC-2 in hemostasis and thrombosis
a novel mechanism of Deep vein thrombosis, whereby CLEC-2 and upregulation of podoplanin (显示 PDPN 蛋白) expression in the venous wall trigger thrombus formation
A reciprocal interaction between CLEC-2 on megakaryocytes and PDPN (显示 PDPN 蛋白) 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 (显示 MKKS 蛋白)).
Data (including data from studies in transgenic mice) suggest that a diverse range of ligands activate platelets through activation/phosphorylation of Cd36 (显示 CD36 蛋白)/GPVI (显示 GP6 蛋白) (glycoprotein VI) and/or Clec-2 (C-type lectin-like receptor-2).
Podoplanin (显示 PDPN 蛋白) and CLEC-2 critically drive the formation and integrity of developing cerebral blood vessels.
PI3K and Tec (显示 NR4A3 蛋白) family kinases play a crucial role in the regulation of platelet activation and Syk (显示 SYK 蛋白) phosphorylation downstream of the CLEC-2 receptor
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-like receptor 2
, C-type lectin-like receptor-2
, C-type lectin domain family 1, member B
, c-type lectin domain family 1 member B-like
, C-type lectin domain containing 9A
, C-type lectin domain family 9 member A