請用此 Handle URI 來引用此文件: http://hdl.handle.net/11455/68432
標題: Enterovirus-Induced miR-141 Contributes to Shutoff of Host Protein Translation by Targeting the Translation Initiation Factor eIF4E
作者: Ho, B.C.
Yu, S.L.
Chen, J.J.W.
Chang, S.Y.
Yan, B.S.
Hong, Q.S.
Singh, S.
Kao, C.L.
Chen, H.Y.
Su, K.Y.
Li, K.C.
Cheng, C.L.
Cheng, H.W.
Lee, J.Y.
Lee, C.N.
Yang, P.C.
關鍵字: poliovirus infection
rna synthesis
virus-replication
microrna
identification
cells
suppression
inhibition
expression
coincides
期刊/報告no:: Cell Host & Microbe, Volume 9, Issue 1, Page(s) 58-69.
摘要: Viruses rely on the host translation machinery to complete their life cycles. Picornaviruses use an internal ribosome entry site to initiate cap-independent protein translation and in parallel host cap-dependent translation is shut off. This process is thought to occur primarily via cleavage of host translation initiation factors eIF4GI and eIF4GII by viral proteases. Here we describe another mechanism whereby miR-141 induced upon enterovirus infection targets the cap-dependent translation initiation factor, eIF4E, for shutoff of host protein synthesis. Knockdown of miR-141 reduces viral propagation, and silencing of eIF4E can completely reverse the inhibitory effect of the miR-141 antagomiR on viral propagation. Ectopic expression of miR-141 promotes the switch from cap-dependent to cap-independent translation. Moreover, we identified a transcription factor, EGR1, which is partly responsible for miR-141 induction in response to enterovirus infection. Our results suggest that upregulation of miR-141 upon enterovirus infection can facilitate viral propagation by expediting the translational switch.
URI: http://hdl.handle.net/11455/68432
ISSN: 1931-3128
文章連結: http://dx.doi.org/10.1016/j.chom.2010.12.001
顯示於類別:期刊論文

文件中的檔案:
沒有與此文件相關的檔案。


在 DSpace 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。