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Putative adhesion molecule that mediates sialic-acid dependent binding to cells. Additionally we are shipping and many more products for this protein.
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Mouse (Murine) Monoclonal Siglece Primary Antibody for CyTOF, FACS - ABIN4899403
Wu, Ren, Chen: Siglec-E Negatively Regulates the Activation of TLR4 by Controlling Its Endocytosis. in Journal of immunology (Baltimore, Md. : 1950) 2016
Show all 2 Pubmed References
The Siglec-E-deficient dendritic cells were defective for TRIF-mediated IFN-beta production in response to E. coli infection.
This study demonstrated that virulent parasite Leishmania donovani (AG83+Sias) establish a unique sialic acids-mediated binding and subsequent phagocytosis in the host cell through the selective exploitation of siglec-1.
new data relating to the structure and function of Siglec-E, the major CD33-related Siglec expressed on mouse neutrophils, monocytes, macrophages, and dendritic cells.
indicate that Siglec-9 affects several different signaling pathways in IL-4-stimulated macrophages, which resulted in enhanced induction of Arg1 in Siglec-9-expressing RAW264 cells
Competitive ELISA assays confirmed the involvement of sulfated epitopes in the affinity between Siglec-E and cruzipain, probably modified by natural protein environment
Data indicate a role for neuraminidase 1 (Neu1) in regulating Siglec E protein-toll-like receptor 4 (TLR4) interaction and endotoxemia.
Siglec-E-deficient macrophages showed a propensity toward a tumor-promoting M2 polarization, indicating a secondary role of CD33-related Siglecs in limiting cancer-promoting inflammation and tumor growth.
Group B Streptococcus engages an inhibitory Siglec through sialic acid mimicry to blunt innate immune and inflammatory responses in vivo.
siglec-E functions as an inhibitory receptor of neutrophils via positive regulation of NADPH oxidase activation and ROS production
These results suggest that sSiglec-9 has an antitumor benefit against MUC1-expressing tumor in the transgenic mice.
Siglec-9 expressed on immune cells may play a role as a potential counterreceptor for MUC1 and that this signaling may be another MUC1-mediated pathway and function in parallel with a growth factor-dependent pathway.
Siglec-E is an important negative regulator of neutrophil recruitment to the lung and beta2 integrin-dependent signaling.
Early murine T-lymphocyte activation is accompanied by a switch from N-Glycolyl- to N-acetyl-neuraminic acid and generation of ligands for siglec-E
Siglec-E is induced in a MyD88-dependent manner. Once up-regulated, it can control TLR-dependent NF-kappaB antiviral responses by directly inhibiting TLR-induced antiviral cytokine production.
Siglec-E interacted with the pathogenic Tulahuen strain, but showed a diminished binding to the Tehuantepec strain of Trypanosoma cruzi
are a family of sialic acid receptor proteins expressed in immune cells, recognize their ligands and play a role in the signal transduction.
Putative adhesion molecule that mediates sialic-acid dependent binding to cells. The sialic acid recognition site may be masked by cis interactions with sialic acids on the same cell surface. In the immune response, may act as an inhibitory receptor upon ligand induced tyrosine phosphorylation by recruiting cytoplasmic phosphatase(s) via their SH2 domain(s) that block signal transduction through dephosphorylation of signaling molecules.
, SIGLEC-like 1
, myeloid inhibitory siglec
, sialic acid binding Ig-like lectin 5
, sialic acid-binding Ig-like lectin 12
, sialic acid-binding Ig-like lectin 5
, sialic acid-binding Ig-like lectin E
, sialic acid-binding Ig-like lectin-like 1
, sialic acid-binding immunoglobulin-like lectin E