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anti-Rat (Rattus) TNFRSF13C Antibodies:
anti-Human TNFRSF13C Antibodies:
anti-Mouse (Murine) TNFRSF13C Antibodies:
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Human Polyclonal TNFRSF13C Primary Antibody for CyTOF, FACS - ABIN4899449
Neri, Kumar, Fulciniti, Vallet, Chhetri, Mukherjee, Tai, Chauhan, Tassone, Venuta, Munshi, Hideshima, Anderson, Raje: Neutralizing B-cell activating factor antibody improves survival and inhibits osteoclastogenesis in a severe combined immunodeficient human multiple myeloma model. in Clinical cancer research : an official journal of the American Association for Cancer Research 2007
Show all 12 Pubmed References
Mouse (Murine) Monoclonal TNFRSF13C Primary Antibody for CyTOF, FACS - ABIN4899448
Benson, Dillon, Castigli, Geha, Xu, Lam, Noelle: Cutting edge: the dependence of plasma cells and independence of memory B cells on BAFF and APRIL. in Journal of immunology (Baltimore, Md. : 1950) 2008
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Mouse (Murine) Monoclonal TNFRSF13C Primary Antibody for Func, FACS - ABIN1169048
Rauch, Tussiwand, Bosco, Rolink: Crucial role for BAFF-BAFF-R signaling in the survival and maintenance of mature B cells. in PLoS ONE 2009
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Mouse (Murine) Monoclonal TNFRSF13C Primary Antibody for FACS, WB - ABIN4282887
Ng, Sutherland, Newton, Qian, Cachero, Scott, Thompson, Wheway, Chtanova, Groom, Sutton, Xin, Tangye, Kalled, Mackay, Mackay: B cell-activating factor belonging to the TNF family (BAFF)-R is the principal BAFF receptor facilitating BAFF costimulation of circulating T and B cells. in Journal of immunology (Baltimore, Md. : 1950) 2004
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Human Monoclonal TNFRSF13C Primary Antibody for FACS - ABIN1169049
Tussiwand, Rauch, Flück, Rolink: BAFF-R expression correlates with positive selection of immature B cells. in European journal of immunology 2012
Mouse (Murine) Monoclonal TNFRSF13C Primary Antibody for CyTOF, ELISA - ABIN4282888
Ma, Zhang, Liu, Wang, Liu, Zhu, Yu, Han, Chen, Hou, Wang, Ma, Shen, Li, Xiao, Wang: B cell activating factor (BAFF) selects IL-10(-)B cells over IL-10(+)B cells during inflammatory responses. in Molecular immunology 2017
Expression patterns of BAFF (show TNFSF13B Antibodies) and its receptor BAFF-R differ according to lupus nephritis class.
Inhibition of ADAM10 (show ADAM10 Antibodies) augments BAFF (show TNFSF13B Antibodies)-dependent survival of primary human B cells, whereas inhibition of ADAM17 (show ADAM17 Antibodies) increases BAFFR expression levels.
Relationships between serum BAFF (show TNFSF13B Antibodies) and BBR expression [(BAFFR, calcium signal modulating cyclophilic ligand interactor (TACI (show TNFRSF13B Antibodies)) and B cell maturation antigen (BCMA (show TNFRSF17 Antibodies))] 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 Antibodies) 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 Antibodies) interactor (TACI (show TNFRSF13B Antibodies)) and B cell maturation antigen (BCMA (show TNFRSF17 Antibodies)) do not change
The expression levels of serum BAFF (show TNFSF13B Antibodies) and the three receptors (TACI (show TNFRSF13B Antibodies), BCMA (show TNFRSF17 Antibodies) 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 Antibodies), not only decreased the apoptosis of B cells and CD8 (show CD8A Antibodies)+ T cells by upregulating the expression of Bcl-2 (show BCL2 Antibodies) and BclxL (show BCL2L1 Antibodies), but also promoted B-cell proliferation in immune thrombocytopenia.
BAFF (show TNFSF13B Antibodies) 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 (show CASP9 Antibodies) correlated with a downregulation of BAFFR (B-cell-activating factor (show TNFSF13B Antibodies) belonging to the TNF (show TNF Antibodies) family (BAFF) receptor) in B cells and ICOS (inducible T-cell costimulator (show ICOS Antibodies)) in T cells.
results indicate that the BAFF (show TNFSF13B Antibodies)-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 Antibodies).
B cell-activating factor (BAFF (show TNFSF13B Antibodies)) upregulates CD28 (show CD28 Antibodies)/B7 and CD40 (show CD40 Antibodies)/CD154 (show CD40LG Antibodies) 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 Antibodies) 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 Antibodies) 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 Antibodies) and two APRIL bind to receptor TACI (show TNFRSF13B Antibodies), BCMA (show TNFRSF17 Antibodies) but not to BAFFR.
Syk (show SYK Antibodies)-deficient B cells require BAFF receptor and CD19 (show CD19 Antibodies)/PI3K signaling for their long-term survival.
In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.
BAFF (show TNFSF13B Antibodies) 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