Hatzoglou A, Roussel J, Bourgeade M F, Rogier E, Madry C, Inoue J, Devergne O, Tsapis A
Laboratory of Experimental Endocrinology, Faculty of Medicine, University of Crete, Heraklion, Greece.
J Immunol. 2000 Aug 1;165(3):1322-30. doi: 10.4049/jimmunol.165.3.1322.
BCMA (B cell maturation) is a nonglycosylated integral membrane type I protein that is preferentially expressed in mature B lymphocytes. Previously, we reported in a human malignant myeloma cell line that BCMA is not primarily present on the cell surface but lies in a perinuclear structure that partially overlaps the Golgi apparatus. We now show that in transiently or stably transfected cells, BCMA is located on the cell surface, as well as in a perinulear Golgi-like structure. We also show that overexpression of BCMA in 293 cells activates NF-kappa B, Elk-1, the c-Jun N-terminal kinase, and the p38 mitogen-activated protein kinase. Coimmunoprecipitation experiments performed in transfected cells showed that BCMA associates with TNFR-associated factor (TRAF) 1, TRAF2, and TRAF3 adaptor proteins. Analysis of deletion mutants of the intracytoplasmic tail of BCMA showed that the 25-aa protein segment, from position 119 to 143, conserved between mouse and human BCMA, is essential for its association with the TRAFs and the activation of NF-kappa B, Elk-1, and c-Jun N-terminal kinase. BCMA belongs structurally to the TNFR family. Its unique TNFR motif corresponds to a variant motif present in the fourth repeat of the TNFRI molecule. This study confirms that BCMA is a functional member of the TNFR superfamily. Furthermore, as BCMA is lacking a "death domain" and its overexpression activates NF-kappa B and c-Jun N-terminal kinase, we can reasonably hypothesize that upon binding of its corresponding ligand BCMA transduces signals for cell survival and proliferation.
BCMA(B细胞成熟抗原)是一种非糖基化的I型整合膜蛋白,在成熟B淋巴细胞中优先表达。此前,我们在一种人类恶性骨髓瘤细胞系中报道,BCMA并非主要存在于细胞表面,而是位于与高尔基体部分重叠的核周结构中。我们现在表明,在瞬时或稳定转染的细胞中,BCMA既位于细胞表面,也存在于核周高尔基体样结构中。我们还表明,BCMA在293细胞中的过表达会激活核因子κB、Elk-1、c-Jun氨基末端激酶和p38丝裂原活化蛋白激酶。在转染细胞中进行的共免疫沉淀实验表明,BCMA与肿瘤坏死因子受体相关因子(TRAF)1、TRAF2和TRAF3衔接蛋白相关联。对BCMA胞质内尾巴缺失突变体的分析表明,小鼠和人类BCMA之间保守的119至143位25个氨基酸的蛋白片段,对于其与TRAFs的关联以及核因子κB、Elk-1和c-Jun氨基末端激酶的激活至关重要。BCMA在结构上属于肿瘤坏死因子受体家族。其独特的肿瘤坏死因子受体基序对应于肿瘤坏死因子受体I分子第四个重复序列中存在的一个变体基序。这项研究证实BCMA是肿瘤坏死因子受体超家族中的一个功能成员。此外,由于BCMA缺乏“死亡结构域”且其过表达会激活核因子κB和c-Jun氨基末端激酶,我们可以合理推测,在其相应配体结合后BCMA会转导细胞存活和增殖的信号。