The objective of this study was to examine the relationship between the expression of
B cell activating factor (BAFF) and BAFF receptor in patients with disease activity
of systemic lupus erythematosus (SLE). Real-time RT-PCR was used to examine BAFF mRNA
expression in peripheral blood monocytes of active and stable SLE patients and
healthy controls. The percentage of BAFF receptor 3 (BR3) on B lymphocytes was
measured by flow cytometry. Soluble BAFF levels in serum were assayed by ELISA.
Microalbumin levels were assayed by an automatic immune analysis machine. BAFF mRNA
and soluble BAFF levels were highest in the active SLE group, followed by the stable
SLE group, and controls (P<0.01). The percentage of BR3 on B lymphocytes was
downregulated in the active SLE group compared with the stable SLE group and controls
(P<0.01). BAFF mRNA levels and soluble BAFF levels were higher in patients who
were positive for proteinuria than in those who were negative (P<0.01). The
percentage of BR3 on B lymphocytes was lower in patients who were positive for
proteinuria than in those who were negative (P<0.01). The BAFF/BR3 axis may be
over-activated in SLE patients. BAFF and BR3 levels may be useful parameters for
evaluating treatment.
Abstract. Bel1, a transactivator of the prototype foamy virus (PFV), plays pivotal roles in the replication of PFV. Previous studies have demonstrated that Bel1 bears a nuclear localization signal (NLS); however, its amino acid sequence remains unclear and the corresponding adaptor importins have not yet been identified. In this study, we inserted various fragments of Bel1 into an EGFP-GST fusion protein and investigated their subcellular localization by fluorescence microscopy. We found that the 215 PRQKRPR 221 fragment, which accords with the consensus sequence K(K/R)X(K/R) of the monopartite NLS, directed the nuclear translocation of Bel1. Point mutation experiments revealed that K 218 , R 219 and R 221 were essential for the nuclear localization of Bel1. The results of GST pull-down assay revealed that the Bel1 peptide 215-221, which bears the NLS, interacted with the nucleocytoplasmic transport receptors, karyopherin alpha 1 (importin alpha 5) (KPNA1), karyopherin alpha 6 (importin alpha 7) (KPNA6) and karyopherin alpha 7 (importin alpha 8) (KPNA7). Finally, in vitro nuclear import assays demonstrated that KPNA1, KPNA6 or KPNA7, along with other necessary nuclear factors, caused
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