The BCMA gene, preferentially expressed during B lymphoid maturation, is bidirectionally transcribed

Abstract

In a previous study of a t(4;16)(q26;p13) translocation, found in a human malignant T-cell lymphoma the BCMA gene, located on chromosome band 16p13.1, has been characterized. In this study we show that the BCMA gene is organized into three exons and its major initiation transcription site is located 69 nucleotides downstream of a TATA box. RNase protection assays demonstrated that the BCMA gene is preferentially expressed in mature B cells, suggesting a role for this gene in the B-cell developmental process. A cDNA complementary to the BCMA cDNA was cloned and sequenced and its presence was assessed by RNase protection assay and anchor-PCR amplification. This antisense-BCMA RNA is transcribed from the same locus as BCMA, and exhibits mRNA characteristic features, e.g. polyadenylation and splicing. It also contains an ORF encoding a putative 115 aa polypeptide, presenting no homology with already known sequences. RNase protection assays demonstrated the simultaneous expression of natural sense and antisense-BCMA transcripts in the majority of human B-cell lines tested.

Circulating levels of B lymphocyte stimulator in patients with rheumatoid arthritis following rituximab treatment: Relationships with B cell depletion, circulating antibodies, and clinical relapse

“…In patients treated more than once, similar rises in serum BLyS levels occurred following each course of BCDT (Figure 2). Because the expression of BLyS receptors is largely restricted to B cells (4,(33)(34)(35)(36)(37), the increase in serum BLyS levels following BCDT may be attributable, at least in part, to the physical loss of BLyS-binding B cells (26). Alternatively, BLyS production may be under homeostatic control from an as-yet-unidentified negative feedback signal from the B cell compartment that is deficient during periods of B cell depletion.…”

Involvement of BAFF and APRIL in the resistance to apoptosis of B-CLL through an autocrine pathway

“…23,26,27 Using RT-PCR, the presence of TACI and BAFF-R mRNAs was found in nearly all leukemic B cells (7 of 9 patients for TACI, 9 of 9 patients for BAFF-R) and in blood-derived normal B cells (5 of 5 donors) (Figure 1), in agreement with the findings of Novak et al 45 The latter showed, in addition, that BCMA mRNA was detected in a subset of B-CLL patients. Moreover, by flow cytometry, they found significant levels of TACI protein at the surfaces of these cells; the lack of suitable antibodies made it difficult to check the membrane expression of BCMA and BAFF-R. 45 These results indicated that leukemic B cells expressed at their surfaces the 2 receptors for BAFF and APRIL.…”

“…22 BAFF, but not APRIL, binds a third receptor named BAFF receptor (BAFF-R or BR3). [23][24][25] BCMA, TACI, and BAFF-R are expressed on normal B lymphocytes 23,26,27 and on a subset of activated T cells for TACI. 27 This system of receptors/ligands is a key factor for B-cell survival and differentiation.…”

Analysis on the association of human BLYS (BAFF, TNFSF13B) polymorphisms with systemic lupus erythematosus and rheumatoid arthritis

“…11 BLyS and a proliferation-inducing ligand (APRIL) bind to B cell maturation antigen (BCMA) and transmembrane activator and CAML-interactor (TACI), 4,12,13 which belong to the tumor necrosis factor receptor superfamily and are mainly expressed in B cells. [14][15][16][17] The intracellular domains of BCMA and TACI associate with TNFreceptor-associated factors (TRAFs), leading to activation of NF-kB. 18,19 Recently, another receptor for BLyS, BAFF-R (also called BR3) was identified, which does not bind to APRIL.…”