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1
Targeted disruption of Traf5 gene causes defects in CD40- and CD27-mediated lymphocyte activation.Traf5基因的靶向破坏导致CD40和CD27介导的淋巴细胞活化缺陷。
Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9803-8. doi: 10.1073/pnas.96.17.9803.
2
CD27, a member of the tumor necrosis factor receptor superfamily, activates NF-kappaB and stress-activated protein kinase/c-Jun N-terminal kinase via TRAF2, TRAF5, and NF-kappaB-inducing kinase.CD27是肿瘤坏死因子受体超家族的一员，通过TRAF2、TRAF5和NF-κB诱导激酶激活NF-κB和应激激活蛋白激酶/c-Jun N端激酶。
J Biol Chem. 1998 May 22;273(21):13353-8. doi: 10.1074/jbc.273.21.13353.
3
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.
4
CD40-mediated signaling in monocytic cells: up-regulation of tumor necrosis factor receptor-associated factor mRNAs and activation of mitogen-activated protein kinase signaling pathways.单核细胞中CD40介导的信号传导：肿瘤坏死因子受体相关因子mRNA的上调及丝裂原活化蛋白激酶信号通路的激活
Int Immunol. 2001 Mar;13(3):273-83. doi: 10.1093/intimm/13.3.273.
5
TRAF5 is a critical mediator of in vitro signals and in vivo functions of LMP1, the viral oncogenic mimic of CD40.TRAF5 是体外信号和 LMP1（CD40 的病毒致癌模拟物）体内功能的关键介质。
Proc Natl Acad Sci U S A. 2009 Oct 6;106(40):17140-5. doi: 10.1073/pnas.0903786106. Epub 2009 Sep 17.
6
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.
7
TNF receptor-associated factor-3 signaling mediates activation of p38 and Jun N-terminal kinase, cytokine secretion, and Ig production following ligation of CD40 on human B cells.肿瘤坏死因子受体相关因子3信号传导介导人B细胞上CD40连接后p38和Jun N端激酶的激活、细胞因子分泌及免疫球蛋白产生。
J Immunol. 1998 Aug 1;161(3):1183-93.
8
Characterization of the intracellular domain of receptor activator of NF-kappaB (RANK). Interaction with tumor necrosis factor receptor-associated factors and activation of NF-kappab and c-Jun N-terminal kinase.核因子κB受体激活剂（RANK）细胞内结构域的特性。与肿瘤坏死因子受体相关因子的相互作用以及核因子κB和c-Jun氨基末端激酶的激活。
J Biol Chem. 1998 Aug 7;273(32):20551-5. doi: 10.1074/jbc.273.32.20551.
9
CD40 activates NF-kappa B and c-Jun N-terminal kinase and enhances chemokine secretion on activated human hepatic stellate cells.CD40激活核因子-κB和c-Jun氨基末端激酶，并增强活化的人肝星状细胞上趋化因子的分泌。
J Immunol. 2001 Jun 1;166(11):6812-9. doi: 10.4049/jimmunol.166.11.6812.
10
TRAF5, a novel tumor necrosis factor receptor-associated factor family protein, mediates CD40 signaling.TRAF5是一种新型肿瘤坏死因子受体相关因子家族蛋白，介导CD40信号传导。
Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9437-42. doi: 10.1073/pnas.93.18.9437.

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Single nucleotide polymorphisms of TRAF2 and TRAF5 gene in ankylosing spondylitis: a case-control study.强直性脊柱炎中TRAF2和TRAF5基因的单核苷酸多态性：一项病例对照研究。
Clin Exp Med. 2021 Nov;21(4):645-653. doi: 10.1007/s10238-021-00719-7. Epub 2021 May 17.
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J Leukoc Biol. 2020 Jun;107(6):907-915. doi: 10.1002/JLB.2MR1119-397R. Epub 2019 Nov 21.
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Signaling control of antibody isotype switching.抗体同种型转换的信号控制。
Adv Immunol. 2019;141:105-164. doi: 10.1016/bs.ai.2019.01.001. Epub 2019 Feb 11.
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Role of TRAFs in Signaling Pathways Controlling T Follicular Helper Cell Differentiation and T Cell-Dependent Antibody Responses.TRAFs 在信号通路中调控滤泡辅助性 T 细胞分化和 T 细胞依赖的抗体应答中的作用。
Front Immunol. 2018 Oct 22;9:2412. doi: 10.3389/fimmu.2018.02412. eCollection 2018.
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Bone Remodeling and the Role of TRAF3 in Osteoclastic Bone Resorption.骨重塑与 TRAF3 在破骨细胞骨吸收中的作用。
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Regulation of Interleukin-6 Receptor Signaling by TNF Receptor-Associated Factor 2 and 5 During Differentiation of Inflammatory CD4 T Cells.肿瘤坏死因子受体相关因子 2 和 5 在炎症性 CD4 T 细胞分化过程中对白细胞介素-6 受体信号的调节。
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Emergence of Members of TRAF and DUB of Ubiquitin Proteasome System in the Regulation of Hypertrophic Cardiomyopathy.泛素蛋白酶体系统中TRAF和DUB成员在肥厚型心肌病调控中的出现
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The oncogenic membrane protein LMP1 sequesters TRAF3 in B-cell lymphoma cells to produce functional TRAF3 deficiency.致癌膜蛋白LMP1在B细胞淋巴瘤细胞中隔离TRAF3，导致功能性TRAF3缺陷。
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本文引用的文献

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ASK1 is essential for JNK/SAPK activation by TRAF2.ASK1对于TRAF2激活JNK/SAPK至关重要。
Mol Cell. 1998 Sep;2(3):389-95. doi: 10.1016/s1097-2765(00)80283-x.
2
Tumor necrosis factor receptor-associated factors (TRAFs)--a family of adapter proteins that regulates life and death.肿瘤坏死因子受体相关因子（TRAFs）——一类调节生死的衔接蛋白家族。
Genes Dev. 1998 Sep 15;12(18):2821-30. doi: 10.1101/gad.12.18.2821.
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Death receptors: signaling and modulation.死亡受体：信号传导与调节
Science. 1998 Aug 28;281(5381):1305-8. doi: 10.1126/science.281.5381.1305.
4
The lymphotoxin beta receptor controls organogenesis and affinity maturation in peripheral lymphoid tissues.淋巴毒素β受体控制外周淋巴组织中的器官发生和亲和力成熟。
Immunity. 1998 Jul;9(1):59-70. doi: 10.1016/s1074-7613(00)80588-9.
5
Characterization of murine CD70 by molecular cloning and mAb.通过分子克隆和单克隆抗体对小鼠CD70进行表征。
Int Immunol. 1998 Apr;10(4):517-26. doi: 10.1093/intimm/10.4.517.
6
CD27, a member of the tumor necrosis factor receptor superfamily, activates NF-kappaB and stress-activated protein kinase/c-Jun N-terminal kinase via TRAF2, TRAF5, and NF-kappaB-inducing kinase.CD27是肿瘤坏死因子受体超家族的一员，通过TRAF2、TRAF5和NF-κB诱导激酶激活NF-κB和应激激活蛋白激酶/c-Jun N端激酶。
J Biol Chem. 1998 May 22;273(21):13353-8. doi: 10.1074/jbc.273.21.13353.
7
Early lethality, functional NF-kappaB activation, and increased sensitivity to TNF-induced cell death in TRAF2-deficient mice.TRAF2基因缺陷型小鼠的早期致死性、功能性核因子κB激活以及对肿瘤坏死因子诱导的细胞死亡敏感性增加。
Immunity. 1997 Nov;7(5):715-25. doi: 10.1016/s1074-7613(00)80391-x.
8
TRAF2 is essential for JNK but not NF-kappaB activation and regulates lymphocyte proliferation and survival.肿瘤坏死因子受体相关因子2（TRAF2）对c-Jun氨基末端激酶（JNK）的激活至关重要，但对核因子κB（NF-κB）的激活并非如此，并且它调节淋巴细胞的增殖和存活。
Immunity. 1997 Nov;7(5):703-13. doi: 10.1016/s1074-7613(00)80390-8.
9
NF-kappaB activation: the I kappaB kinase revealed?核因子-κB激活：IκB激酶被揭示了吗？
Cell. 1997 Oct 31;91(3):299-302. doi: 10.1016/s0092-8674(00)80413-4.
10
Tumor necrosis factor (TNF)-mediated kinase cascades: bifurcation of nuclear factor-kappaB and c-jun N-terminal kinase (JNK/SAPK) pathways at TNF receptor-associated factor 2.肿瘤坏死因子（TNF）介导的激酶级联反应：在肿瘤坏死因子受体相关因子2处核因子-κB和c-Jun氨基末端激酶（JNK/SAPK）途径的分支
Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9792-6. doi: 10.1073/pnas.94.18.9792.

Traf5基因的靶向破坏导致CD40和CD27介导的淋巴细胞活化缺陷。

Targeted disruption of Traf5 gene causes defects in CD40- and CD27-mediated lymphocyte activation.

作者信息

Nakano H, Sakon S, Koseki H, Takemori T, Tada K, Matsumoto M, Munechika E, Sakai T, Shirasawa T, Akiba H, Kobata T, Santee S M, Ware C F, Rennert P D, Taniguchi M, Yagita H, Okumura K

机构信息

Department of Immunology, Juntendo University, School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.

出版信息

Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9803-8. doi: 10.1073/pnas.96.17.9803.

DOI:10.1073/pnas.96.17.9803
PMID:10449775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC22291/
Abstract

TRAF5 [tumor necrosis factor (TNF) receptor-associated factor 5] is implicated in NF-kappaB and c-Jun NH(2)-terminal kinase/stress-activated protein kinase activation by members of the TNF receptor superfamily, including CD27, CD30, CD40, and lymphotoxin-beta receptor. To investigate the functional role of TRAF5 in vivo, we generated TRAF5-deficient mice by gene targeting. Activation of either NF-kappaB or c-Jun NH(2)-terminal kinase/stress-activated protein kinase by tumor necrosis factor, CD27, and CD40 was not abrogated in traf5(-/-) mice. However, traf5(-/-) B cells showed defects in proliferation and up-regulation of various surface molecules, including CD23, CD54, CD80, CD86, and Fas in response to CD40 stimulation. Moreover, in vitro Ig production of traf5(-/-) B cells stimulated with anti-CD40 plus IL-4 was reduced substantially. CD27-mediated costimulatory signal also was impaired in traf5(-/-) T cells. Collectively, these results demonstrate that TRAF5 is involved in CD40- and CD27-mediated signaling.

摘要

肿瘤坏死因子（TNF）受体相关因子5（TRAF5）与TNF受体超家族成员（包括CD27、CD30、CD40和淋巴毒素β受体）介导的核因子κB（NF-κB）及c-Jun氨基末端激酶/应激激活蛋白激酶的激活有关。为了研究TRAF5在体内的功能作用，我们通过基因打靶构建了TRAF5缺陷小鼠。在traf5（-/-）小鼠中，肿瘤坏死因子、CD27和CD40介导的NF-κB或c-Jun氨基末端激酶/应激激活蛋白激酶的激活并未消除。然而，traf5（-/-）B细胞在对CD40刺激的增殖反应以及包括CD23、CD54、CD80、CD86和Fas在内的多种表面分子上调方面存在缺陷。此外，用抗CD40加白细胞介素-4刺激的traf5（-/-）B细胞的体外免疫球蛋白产生显著减少。traf5（-/-）T细胞中CD27介导的共刺激信号也受损。总体而言，这些结果表明TRAF5参与了CD40和CD27介导的信号传导。