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Epidermal Growth Factor Receptor-PI3K Signaling Controls Cofilin Activity To Facilitate Herpes Simplex Virus 1 Entry into Neuronal Cells
http://hdl.handle.net/10069/34599
http://hdl.handle.net/10069/345992c907f6c-2883-4ac2-bc8e-d42896acada2
名前 / ファイル | ライセンス | アクション |
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mBio5_00958-13.pdf (5.6 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2014-07-28 | |||||
タイトル | ||||||
タイトル | Epidermal Growth Factor Receptor-PI3K Signaling Controls Cofilin Activity To Facilitate Herpes Simplex Virus 1 Entry into Neuronal Cells | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Zheng, Kai
× Zheng, Kai× Xiang, Yangfei× Wang, Xiao× Wang, Qiaoli× Zhong, Meigong× Wang, Shaoxiang× Wang, Xiaoyan× Fan, Jianglin× Kitazato, Kaio× Wang, Yifei |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Herpes simplex virus type 1 (HSV-1) establishes latency in neurons and can cause severe disseminated infection with neurological impairment and high mortality. This neurodegeneration is thought to be tightly associated with virus-induced cytoskeleton disruption. Currently, the regulation pattern of the actin cytoskeleton and the involved molecular mechanisms during HSV-1 entry into neurons remain unclear. Here, we demonstrate that the entry of HSV-1 into neuronal cells induces biphasic remodeling of the actin cytoskeleton and an initial inactivation followed by the subsequent activation of cofilin, a member of the actin depolymerizing factor family that is critical for actin reorganization. The disruption of F-actin dynamics or the modulation of cofilin activity by mutation, knockdown, or overexpression affects HSV-1 entry efficacy and virus-mediated cell ruffle formation. Binding of the HSV-1 envelope initiates the epidermal growth factor receptor (EGFR)-phosphatidylinositide 3-kinase (PI3K) signaling pathway, which leads to virus-induced early cofilin phosphorylation and F-actin polymerization. Moreover, the extracellular signal-regulated kinase (ERK) kinase and Rho-associated, coiled-coil-containing protein kinase 1 (ROCK) are recruited as downstream mediators of the HSV-1-induced cofilin inactivation pathway. Inhibitors specific for those kinases significantly reduce the virus infectivity without affecting virus binding to the target cells. Additionally, lipid rafts are clustered to promote EGFR-associated signaling cascade transduction. We propose that HSV-1 hijacks cofilin to initiate infection. These results could promote a better understanding of the pathogenesis of HSV-1-induced neurological diseases. | |||||
書誌情報 |
mBio 巻 5, 号 1, p. e00958-13, 発行日 2014-01-14 |
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出版者 | ||||||
出版者 | American Society for Microbiology | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 21507511 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1128/mBio.00958-13 | |||||
権利 | ||||||
権利情報 | c 2014 Zheng et al. | |||||
権利 | ||||||
権利情報 | This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported license, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | mBio, 5(1), e00958-13; 2014 |