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Inhibition of ADAM10 (Montrer ADAM10 Protéines) augments BAFF (Montrer TNFSF13B Protéines)-dependent survival of primary human B cells, whereas inhibition of ADAM17 (Montrer ADAM17 Protéines) increases BAFFR expression levels.
Relationships between serum BAFF (Montrer TNFSF13B Protéines) and BBR expression [(BAFFR, calcium signal modulating cyclophilic ligand interactor (TACI (Montrer TNFRSF13B Protéines)) and B cell maturation antigen (BCMA (Montrer TNFRSF17 Protéines))] 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 (Montrer TNFSF13B Protéines) 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 (Montrer CAMLG Protéines) interactor (TACI (Montrer TNFRSF13B Protéines)) and B cell maturation antigen (BCMA (Montrer TNFRSF17 Protéines)) do not change
The expression levels of serum BAFF (Montrer TNFSF13B Protéines) and the three receptors (TACI (Montrer TNFRSF13B Protéines), BCMA (Montrer TNFRSF17 Protéines) 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 (Montrer TNFSF13B Protéines), not only decreased the apoptosis of B cells and CD8 (Montrer CD8A Protéines)+ T cells by upregulating the expression of Bcl-2 (Montrer BCL2 Protéines) and BclxL (Montrer BCL2L1 Protéines), but also promoted B-cell proliferation in immune thrombocytopenia.
BAFF (Montrer TNFSF13B Protéines) 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 (Montrer CASP9 Protéines) correlated with a downregulation of BAFFR (B-cell-activating factor (Montrer TNFSF13B Protéines) belonging to the TNF (Montrer TNF Protéines) family (BAFF) receptor) in B cells and ICOS (inducible T-cell costimulator (Montrer ICOS Protéines)) in T cells.
Variants of TNFRSF13C were associated with common variable immunodeficiency.
B cell-activating factor (BAFF (Montrer TNFSF13B Protéines)) upregulates CD28 (Montrer CD28 Protéines)/B7 and CD40 (Montrer CD40 Protéines)/CD154 (Montrer CD40LG Protéines) 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 (Montrer FAS Protéines) 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 (Montrer CXCL13 Protéines) 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 (Montrer TNFSF13B Protéines) and two APRIL bind to receptor TACI (Montrer TNFRSF13B Protéines), BCMA (Montrer TNFRSF17 Protéines) but not to BAFFR.
Syk (Montrer SYK Protéines)-deficient B cells require BAFF receptor and CD19 (Montrer CD19 Protéines)/PI3K signaling for their long-term survival.
In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.
BAFF (Montrer TNFSF13B Protéines) 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