Meili Li
Chinese Academy of Sciences
18 Papers
77 Citations
Meili Li is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Herpes simplex virus & Biology. The author has an hindex of 8, co-authored 13 publications. Previous affiliations of Meili Li include Guangzhou Medical University.
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Papers
The herpes simplex virus 1-encoded envelope glycoprotein B activates NF-κB through the Toll-like receptor 2 and MyD88/TRAF6-dependent signaling pathway.
Mingsheng Cai,Meili Li,Kezhen Wang,Kezhen Wang,Shuai Wang,Shuai Wang,Qiong Lu,Jinghua Yan,Karen L. Mossman,Rongtuan Lin,Chunfu Zheng,Chunfu Zheng +11 more
TL;DR: Results indicate the importance and potency of HSV-1 gB as one of pathogen-associated molecular patterns (PAMPs) molecule recognized by TLR2 with immediate kinetics.
Identification of Nuclear and Nucleolar Localization Signals of Pseudorabies Virus (PRV) Early Protein UL54 Reveals that Its Nuclear Targeting Is Required for Efficient Production of PRV
TL;DR: It is demonstrated that the nuclear targeting of UL54 is required for efficient production of PRV and identified a classical NLS and a genuine NoLS in UL54.
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FTO alleviates cerebral ischemia/reperfusion-induced neuroinflammation by decreasing cGAS mRNA stability in an m6A-dependent manner.
Zhiyong Yu,Yanqing Geng,Yuting Zhang,Yu-Peng Wang,Guoxing You,Mingsheng Cai,Meili Li,Xiao Cheng,Jie Zan +8 more
TL;DR: In this paper , the authors explored whether m6A modification is associated with microglia-mediated inflammation in cerebral I/R injury and its underlying regulatory mechanism using an in vivo mice model of intraluminal middle cerebral artery occlusion/reperfusion (MCAO/R) and in vitro models of primary isolated micro glia and BV2 microglial cells subjected to oxygen-glucose deprivation and reoxygenation (OGD/R).
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Characterization of molecular determinants for nucleocytoplasmic shuttling of PRV UL54.
TL;DR: UL54 shuttles between the nucleus and the cytoplasm via a TAP/NXF1, but not CRM1, dependent nuclear export pathway, and was demonstrated to target to the nucleus through a classic Ran-, importin β1- and α5-dependent nuclear import mechanism.
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Herpesviral infection and Toll-like receptor 2.
TL;DR: This review summarizes and discusses the recent advances about the specific role of TLR2 in triggering inflammatory responses in herpesvirus infection and the consequences of the alarms raised in the host that they are assigned to protect.