• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肿瘤坏死因子受体家族成员BCMA(B细胞成熟抗原)与肿瘤坏死因子受体相关因子(TRAF)1、TRAF2和TRAF3结合,并激活核因子κB、 Elk-1、c-Jun氨基末端激酶和p38丝裂原活化蛋白激酶。

TNF receptor family member BCMA (B cell maturation) associates with TNF receptor-associated factor (TRAF) 1, TRAF2, and TRAF3 and activates NF-kappa B, elk-1, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase.

作者信息

Hatzoglou A, Roussel J, Bourgeade M F, Rogier E, Madry C, Inoue J, Devergne O, Tsapis A

机构信息

Laboratory of Experimental Endocrinology, Faculty of Medicine, University of Crete, Heraklion, Greece.

出版信息

J Immunol. 2000 Aug 1;165(3):1322-30. doi: 10.4049/jimmunol.165.3.1322.

DOI:10.4049/jimmunol.165.3.1322
PMID:10903733
Abstract

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.

摘要

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。

相似文献

1
TNF receptor family member BCMA (B cell maturation) associates with TNF receptor-associated factor (TRAF) 1, TRAF2, and TRAF3 and activates NF-kappa B, elk-1, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase.肿瘤坏死因子受体家族成员BCMA(B细胞成熟抗原)与肿瘤坏死因子受体相关因子(TRAF)1、TRAF2和TRAF3结合,并激活核因子κB、 Elk-1、c-Jun氨基末端激酶和p38丝裂原活化蛋白激酶。
J Immunol. 2000 Aug 1;165(3):1322-30. doi: 10.4049/jimmunol.165.3.1322.
2
Differential requirements for tumor necrosis factor receptor-associated factor family proteins in CD40-mediated induction of NF-kappaB and Jun N-terminal kinase activation.肿瘤坏死因子受体相关因子家族蛋白在CD40介导的核因子κB诱导及Jun N端激酶激活中的差异需求
J Biol Chem. 1999 Aug 6;274(32):22414-22. doi: 10.1074/jbc.274.32.22414.
3
Receptor activator of NF-kappaB recruits multiple TRAF family adaptors and activates c-Jun N-terminal kinase.核因子κB受体激活剂招募多种肿瘤坏死因子受体相关因子家族衔接蛋白并激活c-Jun氨基末端激酶。
FEBS Lett. 1999 Jan 29;443(3):297-302. doi: 10.1016/s0014-5793(98)01731-1.
4
The TRAF family of signal transducers mediates NF-kappaB activation by the TRANCE receptor.信号转导分子的TRAF家族通过TRANCE受体介导核因子κB的激活。
J Biol Chem. 1998 Oct 23;273(43):28355-9. doi: 10.1074/jbc.273.43.28355.
5
An 11-amino acid sequence in the cytoplasmic domain of CD40 is sufficient for activation of c-Jun N-terminal kinase, activation of MAPKAP kinase-2, phosphorylation of I kappa B alpha, and protection of WEHI-231 cells from anti-IgM-induced growth arrest.CD40胞质结构域中的一段11个氨基酸的序列足以激活c-Jun氨基末端激酶、激活丝裂原活化蛋白激酶相关蛋白激酶-2、使IκBα磷酸化,并保护WEHI-231细胞免受抗IgM诱导的生长停滞。
J Immunol. 1999 Apr 15;162(8):4720-30.
6
TNFR-associated factor-3 is associated with BAFF-R and negatively regulates BAFF-R-mediated NF-kappa B activation and IL-10 production.肿瘤坏死因子受体相关因子-3与B细胞活化因子受体相关,并负向调节B细胞活化因子受体介导的核因子κB激活及白细胞介素-10的产生。
J Immunol. 2002 Dec 15;169(12):6883-9. doi: 10.4049/jimmunol.169.12.6883.
7
CD40 signaling through tumor necrosis factor receptor-associated factors (TRAFs). Binding site specificity and activation of downstream pathways by distinct TRAFs.通过肿瘤坏死因子受体相关因子(TRAFs)进行的CD40信号传导。不同TRAFs的结合位点特异性及下游通路的激活。
J Biol Chem. 1999 May 14;274(20):14246-54. doi: 10.1074/jbc.274.20.14246.
8
NF-kappa B-inducing kinase is a common mediator of IL-17-, TNF-alpha-, and IL-1 beta-induced chemokine promoter activation in intestinal epithelial cells.核因子κB诱导激酶是白细胞介素-17、肿瘤坏死因子-α和白细胞介素-1β诱导肠道上皮细胞趋化因子启动子激活的共同介质。
J Immunol. 1999 May 1;162(9):5337-44.
9
TCR-independent CD30 signaling selectively induces IL-13 production via a TNF receptor-associated factor/p38 mitogen-activated protein kinase-dependent mechanism.不依赖TCR的CD30信号传导通过肿瘤坏死因子受体相关因子/p38丝裂原活化蛋白激酶依赖性机制选择性诱导白细胞介素-13的产生。
J Immunol. 2002 Sep 1;169(5):2451-9. doi: 10.4049/jimmunol.169.5.2451.
10
TNF-mediated activation of the stress-activated protein kinase pathway: TNF receptor-associated factor 2 recruits and activates germinal center kinase related.肿瘤坏死因子介导的应激激活蛋白激酶途径的激活:肿瘤坏死因子受体相关因子2招募并激活生发中心激酶相关蛋白。
J Immunol. 1999 Sep 15;163(6):3279-85.

引用本文的文献

1
BCMA CAR-T: From Multiple Myeloma to Light-Chain Amyloidosis.靶向B细胞成熟抗原的嵌合抗原受体T细胞疗法:从多发性骨髓瘤到轻链淀粉样变
Curr Oncol. 2025 Jul 25;32(8):418. doi: 10.3390/curroncol32080418.
2
B cell maturation antigen (BCMA) is dispensable for the survival of long-lived plasma cells.B细胞成熟抗原(BCMA)对于长寿浆细胞的存活并非必需。
Nat Commun. 2025 Aug 2;16(1):7106. doi: 10.1038/s41467-025-62530-2.
3
Resistance Mechanisms to BCMA Targeting Bispecific Antibodies and CAR T-Cell Therapies in Multiple Myeloma.多发性骨髓瘤中针对BCMA的双特异性抗体和CAR T细胞疗法的耐药机制
Cells. 2025 Jul 15;14(14):1077. doi: 10.3390/cells14141077.
4
Integrative Proteomics and Genomics Identify Novel Biomarkers and Therapeutic Targets in Vitiligo via Mendelian Randomization.整合蛋白质组学和基因组学通过孟德尔随机化确定白癜风的新型生物标志物和治疗靶点。
Dermatol Ther (Heidelb). 2025 Jun 19. doi: 10.1007/s13555-025-01448-5.
5
AL Amyloidosis: Current Treatment and Outcomes.轻链型淀粉样变性:当前的治疗方法与治疗结果
Adv Hematol. 2025 Mar 3;2025:7280805. doi: 10.1155/ah/7280805. eCollection 2025.
6
Individualized dynamic risk assessment and treatment selection for multiple myeloma.多发性骨髓瘤的个体化动态风险评估与治疗选择
Br J Cancer. 2025 Jun;132(10):922-936. doi: 10.1038/s41416-025-02987-6. Epub 2025 Apr 1.
7
Similarities and differences of a proliferation-inducing ligand expression in lacrimal gland lesions of patients with IgG4-associated ophthalmic diseases and mucosa-associated lymphoid tissue lymphoma.IgG4相关性眼病患者泪腺病变及黏膜相关淋巴组织淋巴瘤中增殖诱导配体表达的异同
Front Immunol. 2025 Feb 18;16:1514003. doi: 10.3389/fimmu.2025.1514003. eCollection 2025.
8
Survival of Human Bone Marrow Plasma Cells In Vitro Depends on the Support of the Stromal Cells, PI3K, and Canonical NF-kappaB Signaling.人骨髓浆细胞在体外的存活依赖于基质细胞、PI3K和经典NF-κB信号通路的支持。
Eur J Immunol. 2025 Jan;55(1):e202451358. doi: 10.1002/eji.202451358.
9
The Antibody Drug Conjugate, Belantamab-Mafodotin, in the Treatment of Multiple Myeloma: A Comprehensive Review.抗体药物偶联物贝兰他单抗莫福汀治疗多发性骨髓瘤的综合综述
Blood Lymphat Cancer. 2024 Dec 6;14:71-87. doi: 10.2147/BLCTT.S490021. eCollection 2024.
10
Novel Tryptophan Hydroxylase Inhibitor TPT-001 Reverses PAH, Vascular Remodeling, and Proliferative-Proinflammatory Gene Expression.新型色氨酸羟化酶抑制剂TPT-001可逆转肺动脉高压、血管重塑以及增殖-促炎基因表达。
JACC Basic Transl Sci. 2024 Jun 5;9(7):890-902. doi: 10.1016/j.jacbts.2024.04.006. eCollection 2024 Jul.