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the B-cell receptor BR3 modulates cellular branching via Rac1 during neuronal migration
Expression patterns of BAFF (show TNFSF13B Proteins) and its receptor BAFF-R differ according to lupus nephritis class.
Inhibition of ADAM10 (show ADAM10 Proteins) augments BAFF (show TNFSF13B Proteins)-dependent survival of primary human B cells, whereas inhibition of ADAM17 (show ADAM17 Proteins) increases BAFFR expression levels.
Relationships between serum BAFF (show TNFSF13B Proteins) and BBR expression [(BAFFR, calcium signal modulating cyclophilic ligand interactor (TACI (show TNFRSF13B Proteins)) and B cell maturation antigen (BCMA (show TNFRSF17 Proteins))] were determined on B cell subsets, defined using immunoglobulin (Ig)D/CD38. Twenty pre-RTX and 18 rheumatoid arthritis patients relapsing after B cell depletion were included.
Among the BAFF (show TNFSF13B Proteins) receptors in a cohort of rheumatoid arthritis (RA) patients, the AA have shown, by fluorescence activated cell sorter (FACS) analysis of median fluorescence intensity (MFI), that transmembrane activator and calcium-modulating cyclophilin ligand (show CAMLG Proteins) interactor (TACI (show TNFRSF13B Proteins)) and B cell maturation antigen (BCMA (show TNFRSF17 Proteins)) do not change
The expression levels of serum BAFF (show TNFSF13B Proteins) and the three receptors (TACI (show TNFRSF13B Proteins), BCMA (show TNFRSF17 Proteins) and BAFF-R) in non-Hodgkin lymphoma patients were significantly higher than in healthy controls.
Variants in BAFF-R gene is associated with chronic lymphocytic leukemia.
BAFF-R, as the principal receptor of BAFF (show TNFSF13B Proteins), not only decreased the apoptosis of B cells and CD8 (show CD8A Proteins)+ T cells by upregulating the expression of Bcl-2 (show BCL2 Proteins) and BclxL (show BCL2L1 Proteins), but also promoted B-cell proliferation in immune thrombocytopenia.
BAFF (show TNFSF13B Proteins) and BAFF-R are expressed in the thyrocytes derived from patients with either autoimmune thyroid disorders or multinodular goiter, as well in the infiltrating immune cells of Graves' disease and Hashimoto's thyroiditis
There is an increased prevalence of the BAFF-R His159Tyr mutation in patients with Sjogren's syndrome (SS), particularly in those with SS complicated by MALT lymphoma whose disease onset occurred at a younger age.
results indicate that the BAFF (show TNFSF13B Proteins)-BAFFR ligation bridged between microglia and neurons could play a critical neuroprotective role in brain ischemic injuries
These findings elucidate a crucial molecular pathway of B cell selection in the earliest phases of activation by identifying a novel link between B cell receptor affinity and BAFF-R signaling towards Mcl-1 (show MCL1 Proteins).
B cell-activating factor (BAFF (show TNFSF13B Proteins)) upregulates CD28 (show CD28 Proteins)/B7 and CD40 (show CD40 Proteins)/CD154 (show CD40LG Proteins) expression, and promotes the interactions between T and B cells in a BAFF receptor-dependent manner.
conclude that P44S BAFFR mutation does not hinder BAFFR function or enhance B cell activity in MRL/Lpr (show FAS Proteins) and MRL mice and that other susceptibility loci on the MRL background contributed to the hyperactivity of these cells
Results from this study suggest blockade of CXCL13 (show CXCL13 Proteins) and BAFFR together may be an effective therapeutic strategy in preventing salivary hypofunction and reducing autoantibody titers and sialadenitis in patients with Sjogren's syndrome
Heteromers consisting of one BAFF (show TNFSF13B Proteins) and two APRIL bind to receptor TACI (show TNFRSF13B Proteins), BCMA (show TNFRSF17 Proteins) but not to BAFFR.
Syk (show SYK Proteins)-deficient B cells require BAFF receptor and CD19 (show CD19 Proteins)/PI3K signaling for their long-term survival.
In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.
BAFF (show TNFSF13B Proteins) controls neural cell survival through BAFF receptor.
BAFF receptor deficiency limits Murid herpesvirus 4 infection.
B cell-activating factor (BAFF) enhances B-cell survival in vitro and is a regulator of the peripheral B-cell population. Overexpression of Baff in mice results in mature B-cell hyperplasia and symptoms of systemic lupus erythematosus (SLE). Also, some SLE patients have increased levels of BAFF in serum. Therefore, it has been proposed that abnormally high levels of BAFF may contribute to the pathogenesis of autoimmune diseases by enhancing the survival of autoreactive B cells. The protein encoded by this gene is a receptor for BAFF and is a type III transmembrane protein containing a single extracellular cysteine-rich domain. It is thought that this receptor is the principal receptor required for BAFF-mediated mature B-cell survival.
tumor necrosis factor receptor superfamily, member 13C
, tumor necrosis factor receptor superfamily member 13C
, B cell-activating factor receptor
, B-cell-activating factor receptor
, BAFF receptor
, BLyS receptor 3
, B-cell maturation defect 1
, b cell-activating factor receptor