ArticleCytoskeleton (Hoboken, N.J.)2017
Divergent roles of β- and γ-actin isoforms during spread of vaccinia virus.
Article in Cytoskeleton (Hoboken, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Diversity from similarity: cellular strategies for assigning particular identities to actin filaments and networks.Open biology · 2020Article
- Recognition of Apoptotic Cells by Viruses and Cytolytic Lymphocytes: Target Selection in the Fog of War.Viral immunology · 2020Article
- Viral cell-to-cell spread: Conventional and non-conventional ways.Advances in virus research · 2020Review
- Variants in exons 5 and 6 of ACTB cause syndromic thrombocytopenia.Nature communications · 2018Article
- Divergent roles of β- and γ-actin isoforms during spread of vaccinia virus.Cytoskeleton (Hoboken, N.J.) · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Actin is a major component of the cytoskeleton and is present as two isoforms in non-muscle cells: β- and γ-cytoplasmic actin. These isoforms are strikingly conserved, differing by only four N-terminal amino acids. During spread from infected cells, vaccinia virus (VACV) particles induce localized actin nucleation that propel virus to surrounding cells and facilitate cell-to-cell spread of infection. Here we show that virus-tipped actin comets are composed of β- and γ-actin. We employed isoform-specific siRNA knockdown to examine the role of the two isoforms in VACV-induced actin comets. Despite the high level of similarity between the actin isoforms, and their colocalization, VACV-induced actin nucleation was dependent exclusively on β-actin. Knockdown of β-actin led to a reduction in the release of virus from infected cells, a phenotype dependent on virus-induced Arp2/3 complex activity. We suggest that local concentrations of actin isoforms may regulate the activity of cellular actin nucleator complexes.
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