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SIGLECs are members of the immunoglobulin superfamily that are expressed on the cell surface. Additionally we are shipping SIGLEC10 Antibodies (97) and SIGLEC10 Proteins (8) and many more products for this protein.
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Siglec-10 is associated with decreased survival and impaired NK cell function in human hepatocellular carcinoma (HCC).
Siglec-10-VAP-1 (show AOC3 ELISA Kits) interaction seems to mediate lymphocyte adhesion to endothelium
Siglec-10 was demonstrated to be involved in the endocytosis of porcine reproductive and respiratory syndrome virus, confirming the important role of Siglec-10 in virus the entry process.
this study shows that Siglec-G inhibits dendritic cells cross-presentation by impairing such complex formation, and our results add insight into the regulation of cross-presentation in adaptive immunity
The effect for Siglec-G deficiency in B cells results in higher B-1 cell numbers and a robust and preferential increase in oxidation-specific epitopes-specific IgM antibodies, which neutralize oxidized LDL-induced inflammation in vivo.
Aging Siglec-G-deficient and Siglec-G 3/FcgammaRIIb double-deficient mice develop an autoimmune phenotype with elevated autoantibody levels and mild glomerulonephritis.
Deficiency of SIGLEC-G was found to increase susceptibility to develop B-cell lymphoproliferative disorders.
Siglec-G is recruited to the immunological synapse by sialic acid ligands on the Ag-bearing cells, producing a tolerogenic signal involving Lyn (show LYN ELISA Kits) and the proapoptotic factor BIM (show BCL2L11 ELISA Kits) that promotes deletion of the B cell and failure of mice to develop Abs to the Ag upon subsequent challenge.
Siglec-G-CD24 (show CD24 ELISA Kits) axis, controls the severity of GVHD and suggest that enhancing this interaction may represent a novel strategy for mitigating GVHD.
Siglec-G sialic acid-dependent binding to the BCR (show BCR ELISA Kits) is crucial for the B1 cell-restricted inhibitory function of Siglec-G and is regulated in an opposite way to that of the related protein CD22 (Siglec-2 (show CD22 ELISA Kits)) on B cells.
Data indicate that the loss of the inhibitory receptor Siglec-G led to a moderate exacerbation of disease severity and early onset in both collagen-induced arthritis and spontaneous lupus nephritis in MRL/lpr (show FAS ELISA Kits) mice.
Siglec-G inhibits B cell activation (show BLNK ELISA Kits) equally in both B1 & B2 subsets. It is expressed at a relatively constant level in numerous B cell subsets. It may maintain B cell tolerance toward self Ags (show GLA ELISA Kits) in various B cell compartments.
Data reveal a negative feedback loop of RIG-I (show DDX58 ELISA Kits) signaling and identify a Siglec-G-mediated immune evasion pathway exploited by RNA viruses.
SIGLECs are members of the immunoglobulin superfamily that are expressed on the cell surface. Most SIGLECs have 1 or more cytoplasmic immune receptor tyrosine-based inhibitory motifs, or ITIMs. SIGLECs are typically expressed on cells of the innate immune system, with the exception of the B-cell expressed SIGLEC6 (MIM 604405).
sialic acid binding Ig-like lectin 10
, sialic acid-binding Ig-like lectin 10-like
, sialic acid binding Ig-like lectin G
, sialic acid-binding Ig-like lectin 10
, sialic acid binding Ig-like lectin 10 Ig-like lectin 7
, siglec-like gene 2
, siglec-like protein 2