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July 26, 2026Journal of VirologyOpen Access

LncRNA ckATP1A1-AS1 inhibits influenza A virus replication by mediating innate immune responses and suppressing viral nuclear import

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Authors

MFMenglu FanZLZhiyuan LiuLDLulu Deng

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Overview

Randomized trial identifies the lncRNA ckATP1A1-AS1 as a key antiviral factor during IAV infection, suggesting novel therapeutic targets.

Key Points

  • This research aims to explore the role of lncRNA ckATP1A1-AS1 in regulating influenza A virus replication and immune responses.
  • Functional analyses of ckATP1A1-AS1 through overexpression and knockdown experiments.
  • Assessment of type I interferon responses and interactions with viral proteins.
  • Mechanistic studies involving binding assays with importin α5.
  • Overexpression of ckATP1A1-AS1 restricted IAV replication, while its knockdown increased replication.
  • Transcription factor JUN activated ckATP1A1-AS1, enhancing interferon-β expression and related genes.
  • ckATP1A1-AS1 disrupted viral nucleoprotein import, reducing viral polymerase activity.

Cite This Study

Fan et al. (2026) studied this question.

synapsesocial.com/papers/6a65a91fd3aea3239cd7928ehttps://doi.org/10.1128/jvi.00259-26
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