腺病毒E3-6.7K维持钙稳态，防止细胞凋亡和花生四烯酸释放。
Adenovirus E3-6.7K maintains calcium homeostasis and prevents apoptosis and arachidonic acid release.
作者信息
Moise Alexander R, Grant Jason R, Vitalis Timothy Z, Jefferies Wilfred A
机构信息
Biotechnology Laboratory, Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.
出版信息
J Virol. 2002 Feb;76(4):1578-87. doi: 10.1128/jvi.76.4.1578-1587.2002.
Abstract
E3-6.7K is a small and hydrophobic membrane glycoprotein encoded by the E3 region of subgroup C adenovirus. Recently, E3-6.7K has been shown to be required for the downregulation of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptors by the adenovirus E3/10.4K and E3/14.5K complex of proteins. We demonstrate here that E3-6.7K has additional protective roles, independent of other virus proteins. In transfected Jurkat T-cell lymphoma cells, E3-6.7K was found to maintain endoplasmic reticulum-Ca(2+) homeostasis and inhibit the induction of apoptosis by thapsigargin. The presence of E3-6.7K also lead to a reduction in the TNF-induced release of arachidonic acid from transfected U937 human histiocytic lymphoma cells. In addition, E3-6.7K protected cells against apoptosis induced through Fas, TNF receptor, and TRAIL receptors. Therefore, E3-6.7K confers a wide range of protective effects against both Ca(2+) flux-induced and death receptor-mediated apoptosis.
摘要
E3-6.7K是一种由C亚组腺病毒E3区域编码的小的疏水性膜糖蛋白。最近研究表明，腺病毒E3/10.4K和E3/14.5K蛋白复合物下调肿瘤坏死因子（TNF）相关凋亡诱导配体（TRAIL）受体需要E3-6.7K。我们在此证明，E3-6.7K具有独立于其他病毒蛋白的额外保护作用。在转染的Jurkat T细胞淋巴瘤细胞中，发现E3-6.7K可维持内质网-Ca(2+)稳态，并抑制毒胡萝卜素诱导的细胞凋亡。E3-6.7K的存在还导致转染的U937人组织细胞淋巴瘤细胞中TNF诱导的花生四烯酸释放减少。此外，E3-6.7K保护细胞免受通过Fas、TNF受体和TRAIL受体诱导的细胞凋亡。因此，E3-6.7K对Ca(2+)通量诱导的凋亡和死亡受体介导的凋亡均具有广泛的保护作用。
相似文献
1
Adenovirus E3-6.7K maintains calcium homeostasis and prevents apoptosis and arachidonic acid release.腺病毒E3-6.7K维持钙稳态，防止细胞凋亡和花生四烯酸释放。
J Virol. 2002 Feb;76(4):1578-87. doi: 10.1128/jvi.76.4.1578-1587.2002.
2
The adenovirus E3-14.7K protein and the E3-10.4K/14.5K complex of proteins, which independently inhibit tumor necrosis factor (TNF)-induced apoptosis, also independently inhibit TNF-induced release of arachidonic acid.腺病毒E3-14.7K蛋白以及E3-10.4K/14.5K蛋白复合物可独立抑制肿瘤坏死因子（TNF）诱导的细胞凋亡，它们也能独立抑制TNF诱导的花生四烯酸释放。
J Virol. 1996 Aug;70(8):4904-13. doi: 10.1128/JVI.70.8.4904-4913.1996.
3
Identification of a novel immunosubversion mechanism mediated by a virologue of the B-lymphocyte receptor TACI.鉴定由B淋巴细胞受体TACI的一种病毒蛋白介导的新型免疫颠覆机制。
Clin Vaccine Immunol. 2007 Jul;14(7):907-17. doi: 10.1128/CVI.00058-07. Epub 2007 May 30.
4
Adenovirus E3-10.4K/14.5K protein complex inhibits tumor necrosis factor-induced translocation of cytosolic phospholipase A2 to membranes.腺病毒E3-10.4K/14.5K蛋白复合物抑制肿瘤坏死因子诱导的胞质磷脂酶A2向细胞膜的转位。
J Virol. 1997 Apr;71(4):2830-7. doi: 10.1128/JVI.71.4.2830-2837.1997.
5
Inhibition of TRAIL-induced apoptosis and forced internalization of TRAIL receptor 1 by adenovirus proteins.腺病毒蛋白对TRAIL诱导的细胞凋亡的抑制作用以及TRAIL受体1的强制内化
J Virol. 2001 Oct;75(19):8875-87. doi: 10.1128/JVI.75.19.8875-8887.2001.
6
Construction and characterization of E1-minus replication-defective adenovirus vectors that express E3 proteins from the E1 region.表达来自E1区E3蛋白的E1缺失复制缺陷型腺病毒载体的构建与鉴定
Virology. 2002 Sep 15;301(1):99-108. doi: 10.1006/viro.2002.1580.
7
The adenovirus E3/10.4K-14.5K proteins down-modulate the apoptosis receptor Fas/Apo-1 by inducing its internalization.腺病毒E3/10.4K-14.5K蛋白通过诱导凋亡受体Fas/Apo-1内化来下调其表达。
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10072-7. doi: 10.1073/pnas.95.17.10072.
8
Three adenovirus E3 proteins cooperate to evade apoptosis by tumor necrosis factor-related apoptosis-inducing ligand receptor-1 and -2.三种腺病毒E3蛋白协同作用，通过肿瘤坏死因子相关凋亡诱导配体受体-1和-2逃避凋亡。
J Biol Chem. 2001 Feb 2;276(5):3270-8. doi: 10.1074/jbc.M008218200. Epub 2000 Oct 24.
9
Adenovirus E3-6.7K protein is required in conjunction with the E3-RID protein complex for the internalization and degradation of TRAIL receptor 2.腺病毒E3-6.7K蛋白与E3-RID蛋白复合物共同作用，是TRAIL受体2内化和降解所必需的。
J Virol. 2004 Nov;78(22):12297-307. doi: 10.1128/JVI.78.22.12297-12307.2004.
10
Constitutive expression of the adenovirus E3-14.7K protein does not prolong adenovirus vector DNA persistence but protects mice against lipopolysaccharide-induced acute hepatitis.腺病毒E3-14.7K蛋白的组成型表达不会延长腺病毒载体DNA的持久性，但可保护小鼠免受脂多糖诱导的急性肝炎。
Hum Gene Ther. 2002 May 20;13(8):921-33. doi: 10.1089/10430340252939032.
引用本文的文献
1
Oncolytic adenovirus encoding variant interleukin-2 combined with chemotherapy enables PD-L1 inhibition in pancreatic cancer models.编码变体白细胞介素-2的溶瘤腺病毒与化疗联合可在胰腺癌模型中实现PD-L1抑制。
Cancer Immunol Immunother. 2025 Jun 4;74(7):234. doi: 10.1007/s00262-025-04072-6.
2
A Renaissance for Oncolytic Adenoviruses?溶瘤腺病毒的复兴？
Viruses. 2023 Jan 26;15(2):358. doi: 10.3390/v15020358.
3
P2Y2 purinergic receptor modulates virus yield, calcium homeostasis, and cell motility in human cytomegalovirus-infected cells.P2Y2 嘌呤能受体调节人巨细胞病毒感染细胞中的病毒产量、钙稳态和细胞迁移。
Proc Natl Acad Sci U S A. 2019 Sep 17;116(38):18971-18982. doi: 10.1073/pnas.1907562116. Epub 2019 Sep 3.
4
Molecular Characterization of the Viroporin Function of Foot-and-Mouth Disease Virus Nonstructural Protein 2B.口蹄疫病毒非结构蛋白 2B 的病毒孔蛋白功能的分子特征。
J Virol. 2018 Nov 12;92(23). doi: 10.1128/JVI.01360-18. Print 2018 Dec 1.
5
Classical Swine Fever Virus p7 Protein Interacts with Host Protein CAMLG and Regulates Calcium Permeability at the Endoplasmic Reticulum.经典猪瘟病毒 p7 蛋白与宿主蛋白 CAMLG 相互作用并调节内质网钙离子通透性。
Viruses. 2018 Aug 28;10(9):460. doi: 10.3390/v10090460.
6
Viruses as modulators of mitochondrial functions.作为线粒体功能调节因子的病毒
Adv Virol. 2013;2013:738794. doi: 10.1155/2013/738794. Epub 2013 Oct 24.
7
No evidence of a death-like function for species B1 human adenovirus type 3 E3-9K during A549 cell line infection.在A549细胞系感染过程中，未发现B1亚群3型人腺病毒E3-9K具有类似死亡的功能的证据。
BMC Res Notes. 2012 Aug 11;5:429. doi: 10.1186/1756-0500-5-429.
8
The Biology of TRAIL and the Role of TRAIL-Based Therapeutics in Infectious Diseases.肿瘤坏死因子相关凋亡诱导配体（TRAIL）的生物学特性及其基于TRAIL的疗法在传染病中的作用
Antiinfect Agents Med Chem. 2009 Apr 1;8(2):87-101. doi: 10.2174/187152109787846060.
9
Inhibition of apoptosis in Cryptosporidium parvum-infected intestinal epithelial cells is dependent on survivin.微小隐孢子虫感染的肠上皮细胞中凋亡的抑制依赖于生存素。
Infect Immun. 2008 Aug;76(8):3784-92. doi: 10.1128/IAI.00308-08. Epub 2008 Jun 2.
10
Identification of a novel immunosubversion mechanism mediated by a virologue of the B-lymphocyte receptor TACI.鉴定由B淋巴细胞受体TACI的一种病毒蛋白介导的新型免疫颠覆机制。
Clin Vaccine Immunol. 2007 Jul;14(7):907-17. doi: 10.1128/CVI.00058-07. Epub 2007 May 30.
本文引用的文献
1
Inhibition of TRAIL-induced apoptosis and forced internalization of TRAIL receptor 1 by adenovirus proteins.腺病毒蛋白对TRAIL诱导的细胞凋亡的抑制作用以及TRAIL受体1的强制内化
J Virol. 2001 Oct;75(19):8875-87. doi: 10.1128/JVI.75.19.8875-8887.2001.
2
Unmodified calcium concentrations in tumour necrosis factor receptor subtype-mediated apoptotic cell death.
Mol Cell Biochem. 2000 Aug;211(1-2):19-26. doi: 10.1023/a:1007189911897.
3
Three adenovirus E3 proteins cooperate to evade apoptosis by tumor necrosis factor-related apoptosis-inducing ligand receptor-1 and -2.三种腺病毒E3蛋白协同作用，通过肿瘤坏死因子相关凋亡诱导配体受体-1和-2逃避凋亡。
J Biol Chem. 2001 Feb 2;276(5):3270-8. doi: 10.1074/jbc.M008218200. Epub 2000 Oct 24.
4
Activation of heat-shock response by an adenovirus is essential for virus replication.腺病毒激活热休克反应对病毒复制至关重要。
Nature. 2000 Sep 14;407(6801):207-11. doi: 10.1038/35025102.
5
Adeno-associated virus type 2 Rep78 induces apoptosis through caspase activation independently of p53.2型腺相关病毒Rep78通过激活半胱天冬酶诱导细胞凋亡，且不依赖于p53。
J Virol. 2000 Oct;74(20):9441-50. doi: 10.1128/jvi.74.20.9441-9450.2000.
6
Slow rise of Ca2+ and slow release of reactive oxygen species are two cross-talked events important in tumour necrosis factor-alpha-mediated apoptosis.
Free Radic Res. 2000 Sep;33(3):295-304. doi: 10.1080/10715760000301461.
7
Cross-talk between two cysteine protease families. Activation of caspase-12 by calpain in apoptosis.两个半胱氨酸蛋白酶家族之间的相互作用。钙蛋白酶在凋亡过程中对caspase-12的激活。
J Cell Biol. 2000 Aug 21;150(4):887-94. doi: 10.1083/jcb.150.4.887.
8
Changes in endoplasmic reticulum luminal environment affect cell sensitivity to apoptosis.内质网腔环境的变化影响细胞对凋亡的敏感性。
J Cell Biol. 2000 Aug 21;150(4):731-40. doi: 10.1083/jcb.150.4.731.
9
NAIP interacts with hippocalcin and protects neurons against calcium-induced cell death through caspase-3-dependent and -independent pathways.神经元凋亡抑制蛋白（NAIP）与海马钙结合蛋白相互作用，并通过半胱天冬酶-3依赖性和非依赖性途径保护神经元免受钙诱导的细胞死亡。
EMBO J. 2000 Jul 17;19(14):3597-607. doi: 10.1093/emboj/19.14.3597.
10
A selective requirement for elevated calcium in DNA degradation, but not early events in anti-Fas-induced apoptosis.DNA降解过程中对升高钙水平存在选择性需求，但在抗Fas诱导的细胞凋亡早期事件中并非如此。
J Biol Chem. 2000 Sep 29;275(39):30586-96. doi: 10.1074/jbc.M004058200.
Zotero 插件