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Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein
09:39

Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein

Published on: April 21, 2015

[Screening cellular proteins interacted with M2 protein of influenza A virus by coimmunoprecipitation]

Yaodong Li1, Zhenhong Guan, Jinghua Yan

  • 1Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China. liyaodong@im.ac.cn

Wei Sheng Wu Xue Bao = Acta Microbiologica Sinica
|October 20, 2009
PubMed
Abstract

Insights

This study identified cellular proteins interacting with influenza A M2 protein (A/M2). Key interactions include ataxin 10, potentially explaining ataxia after flu infection, and eukaryotic initiation factors (eIFs), suggesting A/M2

Area of Science:

  • Virology
  • Molecular Biology
  • Neuroscience

Context:

  • Influenza A virus M2 protein (A/M2) plays a crucial role in viral replication and pathogenesis.
  • The cellular interactome of A/M2 is not fully elucidated, hindering a complete understanding of its function.
  • Acute cerebellar ataxia is a rare but serious neurological complication associated with influenza infections and vaccinations.

Purpose:

  • To identify cellular proteins that interact with the influenza A virus M2 protein (A/M2).
  • To investigate potential mechanisms linking influenza A virus infection to neurological symptoms like ataxia.
  • To explore the role of A/M2 in viral protein synthesis regulation.

Summary:

  • Influenza A M2 protein (A/M2) was expressed as a Flag fusion protein in HEK 293T cells.
  • Co-purification with anti-Flag M2 agarose beads followed by mass spectrometry identified interacting proteins.
  • Ataxin 10 and eukaryotic initiation factors (eIFs) were identified as A/M2 interacting partners.

Impact:

  • The interaction between Ataxin 10 and A/M2 provides a molecular basis for understanding influenza-associated acute cerebellar ataxia.
  • The interaction of A/M2 with eIFs suggests a role for the M2 protein in regulating influenza virus protein synthesis.
  • These findings contribute to understanding influenza virus pathogenesis and potential therapeutic targets.

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