Correction: SARS Coronavirus 3b Accessory Protein Modulates Transcriptional Activity of RUNX1b Public Deposited

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Creator
  • Bhavna Varshney
    • Other Affiliation: Virology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India
  • Sudhakar Agnihotram
    • Other Affiliation: Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America
  • Yee-Joo Tan
    • Other Affiliation: Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
  • Ralph Baric
    • Other Affiliation: Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America
  • Sunil K. Lal
    • Other Affiliation: Virology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India
Abstract
  • BackgroundThe causative agent of severe acute respiratory syndrome, SARS coronavirus (SARS-CoV) genome encodes several unique group specific accessory proteins with unknown functions. Among them, accessory protein 3b (also known as ORF4) was lately identified as one of the viral interferon antagonist. Recently our lab uncovered a new role for 3b in upregulation of AP-1 transcriptional activity and its downstream genes. Thus, we believe that 3b might play an important role in SARS-CoV pathogenesis and therefore is of considerable interest. The current study aims at identifying novel host cellular interactors of the 3b protein.Methodology/Principal FindingsIn this study, using yeast two-hybrid and co-immunoprecipitation techniques, we have identified a host transcription factor RUNX1b (Runt related transcription factor, isoform b) as a novel interacting partner for SARS-CoV 3b protein. Chromatin immunoprecipitaion (ChIP) and reporter gene assays in 3b expressing jurkat cells showed recruitment of 3b on the RUNX1 binding element that led to an increase in RUNX1b transactivation potential on the IL2 promoter. Kinase assay and pharmacological inhibitor treatment implied that 3b also affect RUNX1b transcriptional activity by regulating its ERK dependent phosphorylation levels. Additionally, mRNA levels of MIP-1α, a RUNX1b target gene upregulated in SARS-CoV infected monocyte-derived dendritic cells, were found to be elevated in 3b expressing U937 monocyte cells.Conclusions/SignificanceThese results unveil a novel interaction of SARS-CoV 3b with the host factor, RUNX1b, and speculate its physiological relevance in upregulating cytokines and chemokine levels in state of SARS virus infection.
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  • Article
Rights statement
  • In Copyright
Journal title
  • PLoS ONE
Journal volume
  • 7
Journal issue
  • 1
Page start
  • 1
Page end
  • 9
Language
  • English
ISSN
  • 1932-6203
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