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Citation: Reis AL, McCauley JW (2013) The Influenza Virus Protein PB1-F2 Interacts with IKKβ and Modulates NF-κB Signalling. PLoS ONE 8(5): e63852. doi:10.1371/journal.pone.0063852
Abstract
PB1-F2, a protein encoded by a second open reading frame of the influenza virus RNA segment 2, has emerged as a modulator of lung inflammatory responses but the molecular mechanisms underlying this are only poorly understood. Here we show that PB1-F2 inhibits the activation of NF-κB dependent signalling pathways in luciferase reporter assays. PB1-F2 proteins from four different viruses interact with IKKβ in yeast two-hybrid assays and by co-immunoprecipitation. PB1-F2 expression did not inhibit IKKβ kinase activity or NF-κB translocation into the nucleus, but NF-κB binding to DNA was severely impaired in PB1-F2 transfected cells as assessed by Electrophoretic Mobility Shift Assay. Neither the N-terminal 57 amino acid truncated forms nor the C-terminus of PB1-F2 were able to inhibit NF-κB dependent signalling, indicating that the full length protein is necessary for the inhibition.
Citation: Reis AL, McCauley JW (2013) The Influenza Virus Protein PB1-F2 Interacts with IKKβ and Modulates NF-κB Signalling. PLoS ONE 8(5): e63852. doi:10.1371/journal.pone.0063852
Editor: Paul Digard, University of Edinburgh, United Kingdom
Received: January 20, 2013; Accepted: April 7, 2013; Published: May 21, 2013
Copyright: ? 2013 Reis, McCauley. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was funded by the Medical Research Council through programme U117585868. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exists
Abstract
PB1-F2, a protein encoded by a second open reading frame of the influenza virus RNA segment 2, has emerged as a modulator of lung inflammatory responses but the molecular mechanisms underlying this are only poorly understood. Here we show that PB1-F2 inhibits the activation of NF-κB dependent signalling pathways in luciferase reporter assays. PB1-F2 proteins from four different viruses interact with IKKβ in yeast two-hybrid assays and by co-immunoprecipitation. PB1-F2 expression did not inhibit IKKβ kinase activity or NF-κB translocation into the nucleus, but NF-κB binding to DNA was severely impaired in PB1-F2 transfected cells as assessed by Electrophoretic Mobility Shift Assay. Neither the N-terminal 57 amino acid truncated forms nor the C-terminus of PB1-F2 were able to inhibit NF-κB dependent signalling, indicating that the full length protein is necessary for the inhibition.
Citation: Reis AL, McCauley JW (2013) The Influenza Virus Protein PB1-F2 Interacts with IKKβ and Modulates NF-κB Signalling. PLoS ONE 8(5): e63852. doi:10.1371/journal.pone.0063852
Editor: Paul Digard, University of Edinburgh, United Kingdom
Received: January 20, 2013; Accepted: April 7, 2013; Published: May 21, 2013
Copyright: ? 2013 Reis, McCauley. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was funded by the Medical Research Council through programme U117585868. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exists