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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 Proteins (23) and many more products for this protein.
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BAFF (show TNFSF13B ELISA Kits)-induced processing of BAFFR (show TNFRSF13C ELISA Kits) regulates BAFF (show TNFSF13B ELISA Kits)-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 ELISA Kits) and the three receptors (TACI, BCMA (show TNFRSF17 ELISA Kits) and BAFF-R (show TNFRSF13C ELISA Kits)) 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 ELISA Kits)), 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 ELISA Kits)-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 ELISA Kits)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 ELISA Kits) 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 ELISA Kits) following TLR stimulation, and TACI- / - mice had undetectable basal serum concentrations of IL-10 (show IL10 ELISA Kits).
Data show that production of autoantibodies in B cell-activating factor (show TNFSF13B ELISA Kits) of the TNF (show TNF ELISA Kits) family (BAFF (show TNFSF13B ELISA Kits)) is dependent on tumor necrosis factor (show TNF ELISA Kits) receptor superfamily, member 13b protein (TACI) expression by B cells.
Taci (-/-) mice and BAFF (show TNFSF13B ELISA Kits) transgenic mice both develop signs of human Systemic Lupus Erythematosus.
Elimination of B lymphocyte stimulator (show TNFSF13B ELISA Kits) 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 ELISA Kits) and two APRIL bind to receptor TACI, BCMA (show TNFRSF17 ELISA Kits) but not to BAFFR (show TNFRSF13C ELISA Kits).
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