ArticleJournal of virology2007
Expression of rotavirus NSP4 alters the actin network organization through the actin remodeling protein cofilin.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- Viroporin activity is necessary for intercellular calcium signals that contribute to viral pathogenesis.Science advances · 2025Article
- The Role of the Host Cytoskeleton in the Formation and Dynamics of Rotavirus Viroplasms.Viruses · 2024Review
- Rotavirus induces intercellular calcium waves through ADP signaling.Science (New York, N.Y.) · 2020Article
- The C Terminus of Rotavirus VP4 Protein Contains an Actin Binding Domain Which Requires Cooperation with the Coiled-Coil Domain for Actin Remodeling.Journal of virology · 2019Article
- Prion-like protein aggregates exploit the RHO GTPase to cofilin-1 signaling pathway to enter cells.The EMBO journal · 2018Article
- Rotavirus NSP4Virus genes · 2017Article
- Human metapneumovirus Induces Reorganization of the Actin Cytoskeleton for Direct Cell-to-Cell Spread.PLoS pathogens · 2016Article
- The epidermal growth factor receptor regulates cofilin activity and promotes transmissible gastroenteritis virus entry into intestinal epithelial cells.Oncotarget · 2016Article
- Pathophysiological Consequences of Calcium-Conducting Viroporins.Annual review of virology · 2015Review
- The Diverse Forms of Lactose Intolerance and the Putative Linkage to Several Cancers.Nutrients · 2015Review
- Article
- Mutational analysis of the rotavirus NSP4 enterotoxic domain that binds to caveolin-1.Virology journal · 2013Article
- Alphaherpesviral US3 kinase induces cofilin dephosphorylation to reorganize the actin cytoskeleton.Journal of virology · 2013Article
- Autophagy hijacked through viroporin-activated calcium/calmodulin-dependent kinase kinase-β signaling is required for rotavirus replication.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Rotavirus non-structural proteins: structure and function.Current opinion in virology · 2012Review
- Rotavirus infection of cells in culture induces activation of RhoA and changes in the actin and tubulin cytoskeleton.PloS one · 2012Article
- Review
- Rotavirus infection activates the UPR but modulates its activity.Virology journal · 2011Article
- Subversion of the actin cytoskeleton during viral infection.Nature reviews. Microbiology · 2011Review
- Conformational Differences Unfold a Wide Range of Enterotoxigenic Abilities Exhibited by rNSP4 Peptides from Different Rotavirus Strains.The open virology journal · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Rotavirus is a major cause of infantile gastroenteritis with a multifactorial pathogenesis. As with many other pathogens, rotavirus infection and replication leads to rearrangement of the cytoskeleton with disorganization of cytoskeletal elements such as actin and cytokeratin through a calcium-dependent process that has not been fully characterized. The rotavirus enterotoxin NSP4, shown previously to elevate intracellular calcium levels when added exogenously as well as when expressed intracellularly, is a key player in intracellular calcium regulation during rotavirus infection. Here, we investigated the role NSP4 may play in actin rearrangement. Expression of NSP4 fused to enhanced green fluorescent protein (NSP4-EGFP), but not expression of EGFP alone, caused stabilization of long cellular projections in fully confluent HEK 293 cells. Cells expressing NSP4-EGFP for 24 h were also resistant to cell rounding induced by cytochalasin D. Quantification of filamentous actin (F-actin) content by using rhodamine-conjugated phalloidin and flow cytometry showed an elevated F-actin content in NSP4-EGFP-expressing and rotavirus-infected cells in comparison with that in nonexpressing and noninfected cells. Normalization of intracellular calcium levels prevented alterations of F-actin content. Observed changes in F-actin amounts correlated with the increased activation of the actin-remodeling protein cofilin. These calcium-dependent actin rearrangements induced by intracellular NSP4 expression may contribute to rotavirus pathogenesis by interfering with cellular processes dependent on subcortical actin remodeling, including ion transport and viral release.
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Registered trials
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.