The eEF1A Proteins: At the Crossroads of Oncogenesis, Apoptosis, and Viral Infections.
The eEF1A Proteins: At the Crossroads of Oncogenesis, Apoptosis, and Viral Infections.
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DOI：
10.3389/fonc.2015.00075
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发表时间：
2015
影响因子：
4.7
通讯作者：
Herbein G
中科院分区：
文献类型：
--
作者：
Abbas W;Kumar A;Herbein G
真核细胞翻译延长因子1α，eEF1A1和eEF1A2，不仅是翻译因子，而且是在乳腺癌、卵巢癌和肺癌等人类肿瘤中高表达的多效性蛋白。EEF1A1调节细胞骨架，表现出伴侣样活性，并控制细胞增殖和细胞死亡。相反，eEF1A2蛋白有利于肿瘤的发生，因为eEF1A2的过度表达会导致细胞转化，并在裸鼠体内产生肿瘤。EEF1A2蛋白刺激磷脂信号转导，激活Akt依赖的细胞迁移和肌动蛋白重塑，最终有利于肿瘤的发生。相反，eEF1A蛋白的失活会导致免疫缺陷、神经和肌肉缺陷，并有利于细胞凋亡。最后，eEF1A蛋白与几种病毒蛋白相互作用，导致病毒复制增强，细胞凋亡减少，细胞转化增加。本文综述了eEF1a蛋白的最新研究结果，表明eEF1a蛋白通过促进肿瘤发生、抑制细胞凋亡和增强病毒致病作用，在多种人类疾病中发挥重要作用。
Eukaryotic translation elongation factors 1 alpha, eEF1A1 and eEF1A2, are not only translation factors but also pleiotropic proteins that are highly expressed in human tumors, including breast cancer, ovarian cancer, and lung cancer. eEF1A1 modulates cytoskeleton, exhibits chaperone-like activity and also controls cell proliferation and cell death. In contrast, eEF1A2 protein favors oncogenesis as shown by the fact that overexpression of eEF1A2 leads to cellular transformation and gives rise to tumors in nude mice. The eEF1A2 protein stimulates the phospholipid signaling and activates the Akt-dependent cell migration and actin remodeling that ultimately favors tumorigenesis. In contrast, inactivation of eEF1A proteins leads to immunodeficiency, neural and muscular defects, and favors apoptosis. Finally, eEF1A proteins interact with several viral proteins resulting in enhanced viral replication, decreased apoptosis, and increased cellular transformation. This review summarizes the recent findings on eEF1A proteins indicating that eEF1A proteins play a critical role in numerous human diseases through enhancement of oncogenesis, blockade of apoptosis, and increased viral pathogenesis.
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影响因子：
4.8
作者：
Abbas W;Dichamp I;Herbein G
通讯作者：
Herbein G
影响因子：
5.4
作者：
Cimarelli, A;Luban, J
通讯作者：
Luban, J
DOI：
10.1111/febs.12554
发表时间：
2013-12
期刊：
The FEBS journal
影响因子：
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作者：
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通讯作者：
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影响因子：
3.9
作者：
Abbott, Catherine M.;Newbery, Helen J.;Soares, Dinesh C.
通讯作者：
Soares, Dinesh C.
影响因子：
16
作者：
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通讯作者：
Veal, Elizabeth A.