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Bcl-XL interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation.Bcl-XL与凋亡蛋白酶激活因子-1相互作用,并抑制凋亡蛋白酶激活因子-1依赖性的半胱天冬酶-9激活。
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Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis.c-Myc诱导的细胞凋亡中CD95受体-配体途径的需求
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Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked.Bcl-2对细胞凋亡的预防作用:线粒体中细胞色素c的释放受阻。
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Fas-induced activation of the cell death-related protease CPP32 Is inhibited by Bcl-2 and by ICE family protease inhibitors.Fas诱导的细胞死亡相关蛋白酶CPP32的激活受到Bcl-2和ICE家族蛋白酶抑制剂的抑制。
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Epstein-Barr virus-coded BHRF1 protein, a viral homologue of Bcl-2, protects human B cells from programmed cell death.爱泼斯坦-巴尔病毒编码的BHRF1蛋白,即Bcl-2的病毒同源物,可保护人类B细胞免于程序性细胞死亡。
Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8479-83. doi: 10.1073/pnas.90.18.8479.
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Epstein-Barr virus BHRF1 protein protects against cell death induced by DNA-damaging agents and heterologous viral infection.爱泼斯坦-巴尔病毒BHRF1蛋白可保护细胞免受DNA损伤剂和异源病毒感染诱导的细胞死亡。
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爱泼斯坦-巴尔病毒基因产物BHRF1对c-Myc诱导的细胞凋亡的抑制作用。

Suppression of c-Myc-induced apoptosis by the Epstein-Barr virus gene product BHRF1.

作者信息

Fanidi A, Hancock D C, Littlewood T D

机构信息

Biochemistry of the Cell Nucleus, Imperial Cancer Research Fund Laboratories, London WC2A 3PX, United Kingdom.

出版信息

J Virol. 1998 Oct;72(10):8392-5. doi: 10.1128/JVI.72.10.8392-8395.1998.

DOI:10.1128/JVI.72.10.8392-8395.1998
PMID:9733891
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC110225/
Abstract

Constitutive expression of the c-myc proto-oncogene in growth factor-deprived fibroblasts promotes proliferation and induces apoptosis. In these cells, apoptosis can be inhibited by survival factors such as insulin-like growth factor I or the bcl-2 proto-oncogene product. Deregulated c-Myc expression is a common feature in Epstein-Barr virus-positive Burkitt's lymphoma in which the c-myc gene is reciprocally translocated and placed under the control of one of the immunoglobulin loci. BHRF1 is an Epstein-Barr virus protein expressed early in the lytic cycle. BHRF1 is a member of the Bcl-2 family and has been shown to suppress apoptosis and to increase cell survival in different settings. In the present study, we report that BHRF1 inhibits c-Myc-induced apoptosis which occurs in the absence of survival factors. It does not, however, affect the capacity of c-Myc to promote cell growth. These findings demonstrate that BHRF1 has not only structural but also functional similarities to Bcl-2.

摘要

在生长因子缺乏的成纤维细胞中,原癌基因c-myc的组成型表达可促进细胞增殖并诱导细胞凋亡。在这些细胞中,细胞凋亡可被诸如胰岛素样生长因子I或原癌基因bcl-2产物等存活因子所抑制。c-Myc表达失调是爱泼斯坦-巴尔病毒(Epstein-Barr virus,EBV)阳性的伯基特淋巴瘤的一个常见特征,在该肿瘤中,c-myc基因发生相互易位并置于一个免疫球蛋白基因座的控制之下。BHRF1是一种在裂解周期早期表达的EBV蛋白。BHRF1是Bcl-2家族的成员,已被证明在不同情况下可抑制细胞凋亡并提高细胞存活率。在本研究中,我们报道BHRF1可抑制在缺乏存活因子时发生的c-Myc诱导的细胞凋亡。然而,它并不影响c-Myc促进细胞生长的能力。这些发现表明,BHRF1不仅在结构上而且在功能上与Bcl-2相似。