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The protein encoded by TNFRSF13B is a lymphocyte-specific member of the tumor necrosis factor (TNF) receptor superfamily. Additionally we are shipping TNFRSF13B Antibodies (174) and TNFRSF13B Kits (21) and many more products for this protein.
Showing 10 out of 23 products:
Human TNFRSF13B Protein expressed in HEK-293 Cells - ABIN1344232
Huard, Tran, Benkhoucha, Manzin-Lorenzi, Santiago-Raber: Selective APRIL blockade delays systemic lupus erythematosus in mouse. in PLoS ONE 2012
BAFF (show TNFSF13B Proteins)-induced processing of BAFFR (show TNFRSF13C Proteins) regulates BAFF (show TNFSF13B Proteins)-mediated B cell responses in a TACI-dependent manner.
results suggest that TACI A181E heterozygosity results in TACI haploinsufficiency with increased susceptibility to pneumococcal infection
The expression levels of serum BAFF (show TNFSF13B Proteins) and the three receptors (TACI, BCMA (show TNFRSF17 Proteins) and BAFF-R (show TNFRSF13C Proteins)) in non-Hodgkin lymphoma patients were significantly higher than in healthy controls.
11% of common variable immunodeficiency patients and 13% of antibody deficiency syndromes patients carried at least one mutated TNFRSF13B allele.
SNPs rs9514828 (BAFF (show TNFSF13B Proteins)), rs3803800 (APRIL) and rs4985726 (TACI) may be associated with the risk of development of B-cell chronic lymphocytic leukemia in a Polish population.
serum levels not associated with disease activity in MPO (show MPO Proteins)-ANCA-associated renal vasculitis
In this review, we aim at giving an insight into the genetics underlying the CVID and particularly at outlining the role of TACI and its relative contribution to the development of CVID-like phenotypes in human.
TNFRSF13B hemizygosity does not recapitulate autoimmune features of common variable immune deficiency -associated C104R and A181E TNFRSF13B mutations, which likely encode dominant negative products, but instead reveals selective TACI haploinsufficiency at later stages of B-cell development.
Common variable immune d (show TNFSF13B Proteins)eficiency patients with heterozygous mutations in TACI alleles increase susceptibility to autoimmune diseases.
The study demonstrated that there is a remarkable interindividual variability of TACI expression in chronic lymphocytic leukemia, although the majority of patients display low to undetectable TACI.
findings highlight a novel mechanism through which BAFF (show TNFSF13B Proteins) promotes humoral autoimmunity via direct, TACI-dependent activation of transitional B cells
this study shows that increased TACI expression in B cells derived from non-obese diabetic mice contributes to the pathogenesis of type 1 diabetes NOD mice
splenic B cells from TACI-deficient (TACI- / -) mice were unable to secrete IL-10 (show IL10 Proteins) following TLR stimulation, and TACI- / - mice had undetectable basal serum concentrations of IL-10 (show IL10 Proteins).
Data show that production of autoantibodies in B cell-activating factor (show TNFSF13B Proteins) of the TNF (show TNF Proteins) family (BAFF (show TNFSF13B Proteins)) is dependent on tumor necrosis factor (show TNF Proteins) receptor superfamily, member 13b protein (TACI) expression by B cells.
Taci (-/-) mice and BAFF (show TNFSF13B Proteins) transgenic mice both develop signs of human Systemic Lupus Erythematosus.
Elimination of B lymphocyte stimulator (show TNFSF13B Proteins) receptor 3 (BR-3) and TACI inhibits the development of SLE in NZM mice.
TACI deficiency has a role in alternatively activated macrophage phenotype and susceptibility to Leishmania infection
Heteromers consisting of one BAFF (show TNFSF13B Proteins) and two APRIL bind to receptor TACI, BCMA (show TNFRSF17 Proteins) but not to BAFFR (show TNFRSF13C Proteins).
Mice lacking TACI are able to clear Citrobacter rodentium, a model pathogen for severe human enteritis, more rapidly than did wild type mice.
The protein encoded by this gene is a lymphocyte-specific member of the tumor necrosis factor (TNF) receptor superfamily. It interacts with calcium-modulator and cyclophilin ligand (CAML). The protein induces activation of the transcription factors NFAT, AP1, and NF-kappa-B and plays a crucial role in humoral immunity by interacting with a TNF ligand. This gene is located within the Smith-Magenis syndrome region on chromosome 17.
transmembrane activator and CAML interactor
, tumor necrosis factor receptor 13B
, tumor necrosis factor receptor superfamily member 13B
, tumor necrosis factor receptor superfamily, member 13B
, transmembrane activator and calcium-modulating and cyclophilin ligand interactor