h-ras exerts opposing effects on type i interferon responses depending on its activation status

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ID: 194869
2017
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Abstract
Using shRNA high-throughput screening, we identified H-Ras as a regulator of antiviral activity, whose depletion could enhance Sindbis virus replication. Further analyses indicated that depletion of H-Ras results in a robust increase in vesicular stomatitis virus infection and 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. As a result, oncogenic H-Ras, H-RasV12, strongly inhibits SeV-induced IFN-β promoter activity and type I interferon signaling. Conversely, the positive effects exerted by H-Ras on RLR signaling are independent of its signaling activity, as a constitutively inactive form of H-Ras, H-RasN17, also positively regulates RLR signaling. Mechanistically, we demonstrate that depletion of H-Ras reduces the formation of MAVS–TNF receptor-associated factor 3 signaling complexes. These results reveal that the H-Ras protein plays a role in promoting MAVS signalosome assembly in the mitochondria, whereas oncogenic H-Ras exerts a negative effect on type I IFN responses.
Reference Key
chen2017frontiersh-ras Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Guann-An Chen;Yun-Ru Lin;Hai-Ting Chung;Lih-Hwa Hwang
Journal sudebno-meditsinskaia ekspertiza
Year 2017
DOI
10.3389/fimmu.2017.00972
URL
http://journal.frontiersin.org/article/10.3389/fimmu.2017.00972/full
Keywords
type i interferon allergy

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