Please use this identifier to cite or link to this item:
https://doi.org/10.3389/fmicb.2020.581867
DC Field | Value | |
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dc.title | Influenza A Virus Nucleoprotein Activates the JNK Stress-Signaling Pathway for Viral Replication by Sequestering Host Filamin A Protein | |
dc.contributor.author | Sharma, A. | |
dc.contributor.author | Batra, J. | |
dc.contributor.author | Stuchlik, O. | |
dc.contributor.author | Reed, M.S. | |
dc.contributor.author | Pohl, J. | |
dc.contributor.author | Chow, V.T.K. | |
dc.contributor.author | Sambhara, S. | |
dc.contributor.author | Lal, S.K. | |
dc.date.accessioned | 2021-08-18T02:51:05Z | |
dc.date.available | 2021-08-18T02:51:05Z | |
dc.date.issued | 2020 | |
dc.identifier.citation | Sharma, A., Batra, J., Stuchlik, O., Reed, M.S., Pohl, J., Chow, V.T.K., Sambhara, S., Lal, S.K. (2020). Influenza A Virus Nucleoprotein Activates the JNK Stress-Signaling Pathway for Viral Replication by Sequestering Host Filamin A Protein. Frontiers in Microbiology 11 : 581867. ScholarBank@NUS Repository. https://doi.org/10.3389/fmicb.2020.581867 | |
dc.identifier.issn | 1664302X | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/197468 | |
dc.description.abstract | Influenza A virus (IAV) poses a major threat to global public health and is known to employ various strategies to usurp the host machinery for survival. Due to its fast-evolving nature, IAVs tend to escape the effect of available drugs and vaccines thus, prompting the development of novel antiviral strategies. High-throughput mass spectrometric screen of host-IAV interacting partners revealed host Filamin A (FLNA), an actin-binding protein involved in regulating multiple signaling pathways, as an interaction partner of IAV nucleoprotein (NP). In this study, we found that the IAV NP interrupts host FLNA-TRAF2 interaction by interacting with FLNA thus, resulting in increased levels of free, displaced TRAF2 molecules available for TRAF2-ASK1 mediated JNK pathway activation, a pathway critical to maintaining efficient viral replication. In addition, siRNA-mediated FLNA silencing was found to promote IAV replication (87% increase) while FLNA-overexpression impaired IAV replication (65% decrease). IAV NP was observed to be a crucial viral factor required to attain FLNA mRNA and protein attenuation post-IAV infection for efficient viral replication. Our results reveal FLNA to be a host factor with antiviral potential hitherto unknown to be involved in the IAV replication cycle thus, opening new possibilities of FLNA-NP interaction as a candidate anti-influenza drug development target. © Copyright © 2020 Sharma, Batra, Stuchlik, Reed, Pohl, Chow, Sambhara and Lal. | |
dc.publisher | Frontiers Media S.A. | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.source | Scopus OA2020 | |
dc.subject | actin-binding proteins | |
dc.subject | host-virus interaction | |
dc.subject | IAV replication | |
dc.subject | next generation anti-influenza target | |
dc.subject | protein-protein interaction | |
dc.type | Article | |
dc.contributor.department | MICROBIOLOGY AND IMMUNOLOGY | |
dc.description.doi | 10.3389/fmicb.2020.581867 | |
dc.description.sourcetitle | Frontiers in Microbiology | |
dc.description.volume | 11 | |
dc.description.page | 581867 | |
Appears in Collections: | Staff Publications Elements |
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