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Expression patterns of BAFF and its receptor BCMA differ according to lupus nephritis class.
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High BCMA expression is associated with primary central nervous system lymphoma.
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soluble BCMA sequesters circulating BAFF, thereby preventing it from performing its signaling to stimulate normal B-cell and plasma cell development, resulting in reduced polyclonal antibody levels in multiple myeloma patients.
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Studied expression of B-cell maturation antigen (BCMA) in osteoblasts and the toxic effect of chromium on its expression; found BCMA is involved in osteogenesis of osteoblasts; chromium downregulates expression of BCMA in osteoblasts.
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BCMA has other contributors for ligands binding except DxL motif. The affinity of BCMA for APRIL higher than for BAFF may be caused by the segment outside of the conservative DxL motif. Moreover, the exposition of new binding modes of BCMA2 interacting with APRIL may establish the foundation of designing novel drugs in the future
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New molecular mechanisms of in vivo Multiple Myeloma (MM) growth and immunosuppression critically dependent on BCMA and APRIL in the Bone marrow microenvironment, further supporting targeting this prominent pathway in MM.
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We have identified a specific serum protein, BCMA, as a novel independent marker for both monitoring and predicting outcomes for MM patients. We have shown that sBCMA is elevated in MM patients, and can be used to follow their disease status, PFS and OS.
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The expression levels of serum BAFF and the three receptors (TACI, BCMA and BAFF-R) in non-Hodgkin lymphoma patients were significantly higher than in healthy controls.
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Decreased BCMA expression on peripheral B cells according to severe disease activity suggests that BCMA plays an important regulating role in B-cell hyperactivity and immune tolerance homeostasis in systemic lupus erythematosus patients
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results suggest that Akt and JNK pathways are involved in the regulation of B-cell maturation antigen (BCMA)
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shedding of BCMA by gamma-secretase controls plasma cells in the bone marrow and yields a potential biomarker for B-cell involvement in human autoimmune diseases
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elevated serum levels in patients with Behcet's disease
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Data show significant differences in expression of tumour necrosis factor family (BAFF) receptors BAFF-R, BCMA and TACI in patients with and without anti-Jo-1 or anti-Ro52/anti-Ro60 autoantibodies.
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High BCMA expression is associated with breast cancer.
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BAFF and APRIL as well as their cognate receptors (BCMA, TACI) correlate with glioma grade. (Meta-analysis)
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The B cell maturation antigen (BCMA) is a tumor necrosis family receptor member that is predominantly expressed on terminally differentiated B cells and, upon binding to its ligands B cell activator of the TNF family and a proliferation inducing ligand.
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Activation of B cells through BCMA regulates spinal cord injury-induced autoimmunity via a proliferation-inducing ligand (APRIL) and B-cell-activating factor (BAFF).
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Data indicate that MAGE3, Survivin and B-cell maturation antigen (BCMA) mRNA-pulsed dendritic cells (DCs) are capable of stimulating tumor-associated antigens (TAA)-specific T-cell responses in multiple myeloma (MM) patients.
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Data indicate that B-cell maturation antigen (BCMA) is a suitable target for chimeric antigen receptor (CAR)-expressing T cells, and adoptive transfer of anti-BCMA-CAR-expressing T cells is a promising new strategy for treating multiple myeloma.
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B-cell maturation antigen (BCMA), an essential membrane protein for maintaining the survival of plasma cells, was identified as a glycoprotein exhibiting complex-type N-glycans at a single N-glycosylation site, asparagine 42.
