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Inhibition of ADAM10 (zeige ADAM10 Proteine) augments BAFF (zeige TNFSF13B Proteine)-dependent survival of primary human B cells, whereas inhibition of ADAM17 (zeige ADAM17 Proteine) increases BAFFR expression levels.
Relationships between serum BAFF (zeige TNFSF13B Proteine) and BBR expression [(BAFFR, calcium signal modulating cyclophilic ligand interactor (TACI (zeige TNFRSF13B Proteine)) and B cell maturation antigen (BCMA (zeige TNFRSF17 Proteine))] 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 (zeige TNFSF13B Proteine) 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 (zeige CAMLG Proteine) interactor (TACI (zeige TNFRSF13B Proteine)) and B cell maturation antigen (BCMA (zeige TNFRSF17 Proteine)) do not change
The expression levels of serum BAFF (zeige TNFSF13B Proteine) and the three receptors (TACI (zeige TNFRSF13B Proteine), BCMA (zeige TNFRSF17 Proteine) 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 (zeige TNFSF13B Proteine), not only decreased the apoptosis of B cells and CD8 (zeige CD8A Proteine)+ T cells by upregulating the expression of Bcl-2 (zeige BCL2 Proteine) and BclxL (zeige BCL2L1 Proteine), but also promoted B-cell proliferation in immune thrombocytopenia.
BAFF (zeige TNFSF13B Proteine) 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.
Expression of mutant caspase-9 (zeige CASP9 Proteine) correlated with a downregulation of BAFFR (B-cell-activating factor (zeige TNFSF13B Proteine) belonging to the TNF (zeige TNF Proteine) family (BAFF) receptor) in B cells and ICOS (inducible T-cell costimulator (zeige ICOS Proteine)) in T cells.
Variants of TNFRSF13C were associated with common variable immunodeficiency.
B cell-activating factor (BAFF (zeige TNFSF13B Proteine)) upregulates CD28 (zeige CD28 Proteine)/B7 and CD40 (zeige CD40 Proteine)/CD154 (zeige CD40LG Proteine) 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 (zeige FAS Proteine) 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 (zeige CXCL13 Proteine) 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 (zeige TNFSF13B Proteine) and two APRIL bind to receptor TACI (zeige TNFRSF13B Proteine), BCMA (zeige TNFRSF17 Proteine) but not to BAFFR.
Syk (zeige SYK Proteine)-deficient B cells require BAFF receptor and CD19 (zeige CD19 Proteine)/PI3K signaling for their long-term survival.
In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.
BAFF (zeige TNFSF13B Proteine) controls neural cell survival through BAFF receptor.
BAFF receptor deficiency limits Murid herpesvirus 4 infection.
Although we have found that TACI is dispensable for controlling B. hermsii infection, mice deficient in BAFFR or BAFF exhibit impairment in B. hermsii-specific IgM responses and clearance of bacteremia.
tnfrsf13c is dispensable for the development of SLE in NZM mice.
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