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Your search keyword '"Meng, Chunchun"' showing total 6 results
Start Over Author "Meng, Chunchun" Journal virology
6 results on '"Meng, Chunchun"'

4. NDV entry into dendritic cells through macropinocytosis and suppression of T lymphocyte proliferation

Author

Tan, Lei, primary, Zhang, Yuqiang, additional, Qiao, Changtao, additional, Yuan, Yanmei, additional, Sun, Yingjie, additional, Qiu, Xusheng, additional, Meng, Chunchun, additional, Song, Cuiping, additional, Liao, Ying, additional, Munir, Muhammad, additional, Nair, Venugopal, additional, Ding, Zhuang, additional, Liu, Xiufan, additional, and Ding, Chan, additional

Published
2018
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5. Newcastle disease virus infection induces activation of the NLRP3 inflammasome

Author

Wang, Binbin, primary, Zhu, Jie, additional, Li, Dandan, additional, Wang, Yang, additional, Zhan, Yuan, additional, Tan, Lei, additional, Qiu, Xusheng, additional, Sun, Yingjie, additional, Song, Cuiping, additional, Meng, Chunchun, additional, Ying, Liao, additional, Xiang, Mao, additional, Meng, Guangxun, additional, and Ding, Chan, additional

Published
2016
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6. Newcastle disease virus induces G 0 /G 1 cell cycle arrest in asynchronously growing cells.

Author

Wang Y, Wang R, Li Y, Sun Y, Song C, Zhan Y, Tan L, Liao Y, Meng C, Qiu X, and Ding C

Subjects
Cell Division genetics, Cell Proliferation, Cyclin D metabolism, DNA Replication, G1 Phase Cell Cycle Checkpoints, HeLa Cells, Host-Pathogen Interactions, Humans, Newcastle disease virus genetics, Signal Transduction, Transcription Factor CHOP metabolism, Cell Cycle, Cell Cycle Checkpoints, Newcastle disease virus physiology, Resting Phase, Cell Cycle, Virus Replication genetics
Abstract

The cell cycle, as a basic cellular process, is conservatively regulated. Consequently, subversion of the host cell replication cycle is a common strategy employed by many viruses to create a cellular environment favorable for viral replication. Newcastle disease virus (NDV) causes disease in poultry and is also an effective oncolytic agent. However, the effects of NDV infection on cell cycle progression are unknown. In this study, we showed that NDV replication in asynchronized cells resulted in the accumulation of infected cells in the G 0 /G 1 phase of the cell cycle, which benefitted the proliferation of NDV. Examination of various cell cycle-regulatory proteins showed that expression of cyclin D1, was significantly reduced following NDV infection. Importantly, the decreased expression of cyclin D1 was reversed by inhibition of CHOP expression, indicating that induction of the PERK-eIF-2a-ATF4-CHOP signaling pathway was involved in the G 0 /G 1 phase cell cycle arrest observed following NDV infection., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Published
2018
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