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An Expression of nc886, a Novel Non-coding RNA, Enhances Hepatitis B Virus Replication

Authors
Kwon, Hyeon-Joong; Jung, Jaesung; Kim, Kyongmin
Department
Department of Microbiology, Ajou University School of Medicine
Abstract
Non-protein-coding RNAs (ncRNAs) including classic ncRNAs such as tRNAs, small ncRNAs such as microRNAs (miRs), and long ncRNA, longer than 200 nucleotides (nts) in length, have been found to regulate the expressions of host and viral genes and the virus-host interactions. 101 nts long nc886, previously named as pre-miR-886 or vtRNA2-1, has recently been identified as a novel ncRNA which binds and naturally represses protein kinase R (PKR). The tumor surveillance model of nc886-PKR pathway had been proposed. Although interferon inhibits hepatitis B virus (HBV) replication through PKR activation, roles of nc886 on HBV replication has never been investigated. Since it had been shown that nc886 is absent or non-detectable in HepG2 cells, effects of nc886 on HBV replication in HepG2-derived HBV replicating cells were examined. Exogenous expression of nc886 in HepG2.2.15 cells, the HepG2-derived HBV replicating stable cells, significantly increased HBV replication. Through an exogenous expression of nc886 in HepG2 cells, HBV replication of HBV X protein deficient mutant was also rescued almost to that of HBV WT. Taken together, we suggest that nc886 may up-regulate HBV replication through PKR inhibition regardless of presence or absence of HBx in HepG2 cells.
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