<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Havranek KE</submitter><funding>National Center for Advancing Translational Sciences</funding><funding>National Institutes of Health</funding><pagination>367</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7996929</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(3)</volume><pubmed_abstract>In recent years, transcriptome profiling studies have identified changes in host splicing patterns caused by viral invasion, yet the functional consequences of the vast majority of these splicing events remain uncharacterized. We recently showed that the host splicing landscape changes during Rift Valley fever virus MP-12 strain (RVFV MP-12) infection of mammalian cells. Of particular interest, we observed that the host mRNA for Rio Kinase 3 (RIOK3) was alternatively spliced during infection. This kinase has been shown to be involved in pattern recognition receptor (PRR) signaling mediated by RIG-I like receptors to produce type-I interferon. Here, we characterize RIOK3 as an important component of the interferon signaling pathway during RVFV infection and demonstrate that RIOK3 mRNA expre</pubmed_abstract><journal>Viruses</journal><pubmed_title>The Atypical Kinase RIOK3 Limits RVFV Propagation and Is Regulated by Alternative Splicing.</pubmed_title><pmcid>PMC7996929</pmcid><funding_grant_id>R03TR002937</funding_grant_id><funding_grant_id>P20GM103546</funding_grant_id><funding_grant_id>R15AI105737</funding_grant_id><pubmed_authors>White LA</pubmed_authors><pubmed_authors>Bisom TC</pubmed_authors><pubmed_authors>Lodmell JS</pubmed_authors><pubmed_authors>Lanchy JM</pubmed_authors><pubmed_authors>Havranek KE</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Atypical Kinase RIOK3 Limits RVFV Propagation and Is Regulated by Alternative Splicing.</name><description>In recent years, transcriptome profiling studies have identified changes in host splicing patterns caused by viral invasion, yet the functional consequences of the vast majority of these splicing events remain uncharacterized. We recently showed that the host splicing landscape changes during Rift Valley fever virus MP-12 strain (RVFV MP-12) infection of mammalian cells. Of particular interest, we observed that the host mRNA for Rio Kinase 3 (RIOK3) was alternatively spliced during infection. This kinase has been shown to be involved in pattern recognition receptor (PRR) signaling mediated by RIG-I like receptors to produce type-I interferon. Here, we characterize RIOK3 as an important component of the interferon signaling pathway during RVFV infection and demonstrate that RIOK3 mRNA expre</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Feb</publication><modification>2025-06-01T01:35:48.142Z</modification><creation>2022-02-09T14:49:48.155Z</creation></dates><accession>S-EPMC7996929</accession><cross_references><pubmed>33652597</pubmed><doi>10.3390/v13030367</doi></cross_references></HashMap>