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疱疹病毒进入介质配体(HVEM-L),一种针对HVEM/TR2的新型配体,可刺激T细胞增殖并抑制HT29细胞生长。

Herpesvirus entry mediator ligand (HVEM-L), a novel ligand for HVEM/TR2, stimulates proliferation of T cells and inhibits HT29 cell growth.

作者信息

Harrop J A, McDonnell P C, Brigham-Burke M, Lyn S D, Minton J, Tan K B, Dede K, Spampanato J, Silverman C, Hensley P, DiPrinzio R, Emery J G, Deen K, Eichman C, Chabot-Fletcher M, Truneh A, Young P R

机构信息

Department of Molecular and Cellular Immunology, SmithKline Beecham Pharmaceuticals, King of Prussia, Pennsylvania 19406, USA.

出版信息

J Biol Chem. 1998 Oct 16;273(42):27548-56. doi: 10.1074/jbc.273.42.27548.

DOI:10.1074/jbc.273.42.27548
PMID:9765287
Abstract

Herpesvirus entry mediator (HVEM), a member of the tumor necrosis factor (TNF) receptor family, mediates herpesvirus entry into cells during infection. Upon overexpression, HVEM activates NF-kappaB and AP-1 through a TNF receptor-associated factor (TRAF)-mediated mechanism. Using an HVEM-Fc fusion protein, we screened soluble forms of novel TNF-related proteins derived from an expressed sequence tag data base. One of these, which we designated HVEM-L, specifically bound to HVEM-Fc with an affinity of 44 nM. This association was confirmed with soluble and membrane forms of both receptor and ligand. HVEM-L mRNA is expressed in spleen, lymph nodes, macrophages, and T cells and encodes a 240-amino acid protein. A soluble, secreted form of the protein stimulates proliferation of T lymphocytes during allogeneic responses, inhibits HT-29 cell growth, and weakly stimulates NF-kappaB-dependent transcription.

摘要

疱疹病毒进入介质(HVEM)是肿瘤坏死因子(TNF)受体家族的成员,在感染期间介导疱疹病毒进入细胞。过表达时,HVEM通过肿瘤坏死因子受体相关因子(TRAF)介导的机制激活核因子κB(NF-κB)和活化蛋白-1(AP-1)。我们使用HVEM-Fc融合蛋白,从表达序列标签数据库中筛选新型TNF相关蛋白的可溶性形式。其中之一,我们将其命名为HVEM-L,以44 nM的亲和力特异性结合HVEM-Fc。受体和配体的可溶性及膜形式均证实了这种结合。HVEM-L mRNA在脾脏、淋巴结、巨噬细胞和T细胞中表达,编码一种240个氨基酸的蛋白质。该蛋白的可溶性分泌形式在同种异体反应期间刺激T淋巴细胞增殖,抑制HT-29细胞生长,并微弱刺激NF-κB依赖性转录。

相似文献

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Herpesvirus entry mediator ligand (HVEM-L), a novel ligand for HVEM/TR2, stimulates proliferation of T cells and inhibits HT29 cell growth.疱疹病毒进入介质配体(HVEM-L),一种针对HVEM/TR2的新型配体,可刺激T细胞增殖并抑制HT29细胞生长。
J Biol Chem. 1998 Oct 16;273(42):27548-56. doi: 10.1074/jbc.273.42.27548.
2
A newly identified member of tumor necrosis factor receptor superfamily (TR6) suppresses LIGHT-mediated apoptosis.肿瘤坏死因子受体超家族的一个新发现成员(TR6)可抑制LIGHT介导的细胞凋亡。
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LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator.肿瘤坏死因子超家族的新成员LIGHT和淋巴毒素α是疱疹病毒进入介质的配体。
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Reciprocal expression of the TNF family receptor herpes virus entry mediator and its ligand LIGHT on activated T cells: LIGHT down-regulates its own receptor.肿瘤坏死因子(TNF)家族受体疱疹病毒侵入介质及其配体LIGHT在活化T细胞上的相互表达:LIGHT下调其自身受体。
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Recombinant, soluble LIGHT (HVEM ligand) induces increased IL-8 secretion and growth arrest in A375 melanoma cells.重组可溶性LIGHT(HVEM配体)可诱导A375黑色素瘤细胞中白细胞介素-8分泌增加并导致生长停滞。
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Herpesvirus entry mediator, a member of the tumor necrosis factor receptor (TNFR) family, interacts with members of the TNFR-associated factor family and activates the transcription factors NF-kappaB and AP-1.疱疹病毒进入介质是肿瘤坏死因子受体(TNFR)家族的成员,它与TNFR相关因子家族的成员相互作用,并激活转录因子核因子κB和活化蛋白-1。
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LIGHT, a novel ligand for lymphotoxin beta receptor and TR2/HVEM induces apoptosis and suppresses in vivo tumor formation via gene transfer.LIGHT,一种淋巴毒素β受体和TR2/HVEM的新型配体,通过基因转移诱导细胞凋亡并抑制体内肿瘤形成。
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Evolutionarily divergent herpesviruses modulate T cell activation by targeting the herpesvirus entry mediator cosignaling pathway.进化上不同的疱疹病毒通过靶向疱疹病毒进入介质共信号通路来调节T细胞活化。
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