Evaluation of the role of H-Ras in the regulation of RLR signaling pathway
博士 === 國立陽明大學 === 微生物及免疫學研究所 === 106 === We have used shRNA high-throughput screening method to screen for the unrevealed potential cellular factors involved in antiviral responses, and identified a proto-oncogene, H-Ras, acting as a positive regulator in antiviral activity, whose depletion could en...
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ndltd-TW-106YM0053800022019-08-31T03:47:38Z http://ndltd.ncl.edu.tw/handle/b985gk Evaluation of the role of H-Ras in the regulation of RLR signaling pathway 闡述H-Ras在RLR訊息傳遞途徑調控中所扮演的角色 Guann-An Chen 陳冠安 博士 國立陽明大學 微生物及免疫學研究所 106 We have used shRNA high-throughput screening method to screen for the unrevealed potential cellular factors involved in antiviral responses, and identified a proto-oncogene, H-Ras, acting as a positive regulator in antiviral activity, whose depletion could enhance Sindbis virus and vesicular stomatitis virus replication. Further analyses indicated that depletion of H-Ras results in a decrease in Sendai virus (SeV)-induced retinoic acid-inducible gene-I-like receptor (RLR) signaling. Interestingly, however, ectopic expression of wild-type H-Ras results in a biphasic mode of RLR signaling regulation: while low-level expression of H-Ras enhances SeV-induced RLR signaling, high-level expression of H-Ras significantly inhibits this signaling. The inhibitory effects correlate with the activation status of H-Ras. Mechanistically, we demonstrate that depletion of H-Ras reduces the formation of MAVS/TRAF3 signaling complexes and oncogenic H-Ras exerts a negative effect on type I IFN (IFN-I) responses. In summary, we have proven the role of H-Ras in the regulation of type I interferon responses; however, the detailed mechanisms remain to be further investigated. Lih-Hwa Hwang 黃麗華 2018 學位論文 ; thesis 66 zh-TW |
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博士 === 國立陽明大學 === 微生物及免疫學研究所 === 106 === We have used shRNA high-throughput screening method to screen for the unrevealed potential cellular factors involved in antiviral responses, and identified a proto-oncogene, H-Ras, acting as a positive regulator in antiviral activity, whose depletion could enhance Sindbis virus and vesicular stomatitis virus replication. Further analyses indicated that depletion of H-Ras results in a decrease in Sendai virus (SeV)-induced retinoic acid-inducible gene-I-like receptor (RLR) signaling. Interestingly, however, ectopic expression of wild-type H-Ras results in a biphasic mode of RLR signaling regulation: while low-level expression of H-Ras enhances SeV-induced RLR signaling, high-level expression of H-Ras significantly inhibits this signaling. The inhibitory effects correlate with the activation status of H-Ras. Mechanistically, we demonstrate that depletion of H-Ras reduces the formation of MAVS/TRAF3 signaling complexes and oncogenic H-Ras exerts a negative effect on type I IFN (IFN-I) responses. In summary, we have proven the role of H-Ras in the regulation of type I interferon responses; however, the detailed mechanisms remain to be further investigated.
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author2 |
Lih-Hwa Hwang |
author_facet |
Lih-Hwa Hwang Guann-An Chen 陳冠安 |
author |
Guann-An Chen 陳冠安 |
spellingShingle |
Guann-An Chen 陳冠安 Evaluation of the role of H-Ras in the regulation of RLR signaling pathway |
author_sort |
Guann-An Chen |
title |
Evaluation of the role of H-Ras in the regulation of RLR signaling pathway |
title_short |
Evaluation of the role of H-Ras in the regulation of RLR signaling pathway |
title_full |
Evaluation of the role of H-Ras in the regulation of RLR signaling pathway |
title_fullStr |
Evaluation of the role of H-Ras in the regulation of RLR signaling pathway |
title_full_unstemmed |
Evaluation of the role of H-Ras in the regulation of RLR signaling pathway |
title_sort |
evaluation of the role of h-ras in the regulation of rlr signaling pathway |
publishDate |
2018 |
url |
http://ndltd.ncl.edu.tw/handle/b985gk |
work_keys_str_mv |
AT guannanchen evaluationoftheroleofhrasintheregulationofrlrsignalingpathway AT chénguānān evaluationoftheroleofhrasintheregulationofrlrsignalingpathway AT guannanchen chǎnshùhraszàirlrxùnxīchuándìtújìngdiàokòngzhōngsuǒbànyǎndejiǎosè AT chénguānān chǎnshùhraszàirlrxùnxīchuándìtújìngdiàokòngzhōngsuǒbànyǎndejiǎosè |
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1719241700442898432 |