ArticlePLoS pathogens2022
Vimentin inhibits α-tubulin acetylation via enhancing α-TAT1 degradation to suppress the replication of human parainfluenza virus type 3.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Crosstalk between vimentin and keratins in viral infection: Implications across the viral life cycle.Virulence · 2026Review
- Streamlining protocols for the establishment of a physical biobank of respiratory viruses in the Philippines.Journal of translational medicine · 2026Article
- Host factors in parainfluenza virus replication: from entry to innate immunity evasion.Frontiers in immunology · 2026Review
- Peptides targeting RAB11A-FIP2 complex inhibit HPIV3, RSV, and IAV replication as broad-spectrum antivirals.Cell & bioscience · 2025Article
- Tubulin Acetylation: A Critical Regulator of Microtubule Function.Results and problems in cell differentiation · 2025Review
- The α-tubulin acetyltransferase ATAT1: structure, cellular functions, and its emerging role in human diseases.Cellular and molecular life sciences : CMLS · 2024Review
- The molecular biophysics of extracellular vimentin and its role in pathogen-host interactions.Current opinion in cell biology · 2023Review
- Cellular vimentin regulates the infectivity of Newcastle disease virus through targeting of the HN protein.Veterinary research · 2023Article
- Microtubule acetylation dyshomeostasis in Parkinson's disease.Translational neurodegeneration · 2023Review
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously found that, among human parainfluenza virus type 3 (HPIV3) proteins, the interaction of nucleoprotein (N) and phosphoprotein (P) provides the minimal requirement for the formation of cytoplasmic inclusion bodies (IBs), which are sites of RNA synthesis, and that acetylated α-tubulin enhances IB fusion and viral replication. In this study, using immunoprecipitation and mass spectrometry assays, we determined that vimentin (VIM) specifically interacted with the N-P complex of HPIV3, and that the head domain of VIM was responsible for this interaction, contributing to the inhibition of IB fusion and viral replication. Furthermore, we found that VIM promoted the degradation of α-tubulin acetyltransferase 1 (α-TAT1), through its head region, thereby inhibiting the acetylation of α-tubulin, IB fusion, and viral replication. In addition, we identified a 20-amino-acid peptide derived from the head region of VIM that participated in the interaction with the N-P complex and inhibited viral replication. Our findings suggest that VIM inhibits the formation of HPIV3 IBs by downregulating α-tubulin acetylation via enhancing the degradation of α-TAT1. Our work sheds light on a new mechanism by which VIM suppresses HPIV3 replication.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.