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. 2016 May 23;17:390. doi: 10.1186/s12864-016-2739-6

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — Schematic presentation of the Jak/stat pathway genes induced by SAV-3 infection without type I IFN treatment (TO-VS-SAV3) and type I IFN treated cells (TO-VS-IFN/SAV3) infected with SAV3. Note each group is subdivided into type I and II receptors, Jak and tyrosine kinases, negative regulators and signal transducers. a shows that the TO-VS-SAV3 had more type I receptor than the TO-VS-IFN/SAV3 shown in b. Among the type II receptors, the IFNGR1 and IFNGR2 were only reported in the TO-VS-IFN/SAV3 and not in the TO-VS-SAV3 while among the Jaks, Tyk2 was only expressed in the TO-VS-SAV3 and not in TO-VS-IFN/SAV3. For the signal transducer, Stat5B was only expressed in the TO-VS-SAV3 and not in the TO-VS-IFN/SAV3 while Stat6 was only expressed in the TO-VS-IFN/SAV3 and not in the TO-VS-SAV3