ArticleThe Journal of cell biology1995
Cytoskeletal rearrangements and the functional role of T-plastin during entry of Shigella flexneri into HeLa cells.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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.
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Who cites it
55 citing papers in PubMed, 173 citations in OpenAlex.
- Host-pathogen interactions involved in erythrocyte invasion byFrontiers in cellular and infection microbiology · 2025Article
- Pathogenic diversification of the gut commensalInfection and immunity · 2024Article
- Plastin 3 in health and disease: a matter of balance.Cellular and molecular life sciences : CMLS · 2021Review
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- Fungal KATs/KDACs: A New Highway to Better Antifungal Drugs?PLoS pathogens · 2016Review
- Molecular mechanisms of host cytoskeletal rearrangements by Shigella invasins.International journal of molecular sciences · 2014Review
- Article
- Pathogens hijack the epigenome: a new twist on host-pathogen interactions.The American journal of pathology · 2014Review
- Contribution of Crk adaptor proteins to host cell and bacteria interactions.BioMed research international · 2014Review
- Domains of the Shigella flexneri type III secretion system IpaB protein involved in secretion regulation.Infection and immunity · 2010Article
- The extreme C terminus of Shigella flexneri IpaB is required for regulation of type III secretion, needle tip composition, and binding.Infection and immunity · 2010Article
- Small-molecule type III secretion system inhibitors block assembly of the Shigella type III secreton.Journal of bacteriology · 2009Article
- The C-terminus of IpaC is required for effector activities related to Shigella invasion of host cells.Microbial pathogenesis · 2008Article
- PtdIns5P activates the host cell PI3-kinase/Akt pathway during Shigella flexneri infection.The EMBO journal · 2006Article
- Francisella tularensis enters macrophages via a novel process involving pseudopod loops.Infection and immunity · 2005Article
- Abl tyrosine kinases are required for infection by Shigella flexneri.The EMBO journal · 2003Article
- Phagocytosis and intracellular fate of Aspergillus fumigatus conidia in alveolar macrophages.Infection and immunity · 2003Article
- Conversion of PtdIns(4,5)P(2) into PtdIns(5)P by the S.flexneri effector IpgD reorganizes host cell morphology.The EMBO journal · 2002Article
- Initial steps of Shigella infection depend on the cholesterol/sphingolipid raft-mediated CD44-IpaB interaction.The EMBO journal · 2002Article
- Chlamydia trachomatis induces remodeling of the actin cytoskeleton during attachment and entry into HeLa cells.Infection and immunity · 2002Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shigella flexneri is an enteroinvasive bacterium which causes bacillary dysentery in humans. A major feature of its pathogenic potential is the capacity to invade epithelial cells. Shigella entry into epithelial cells is considered a parasite-induced internalization process requiring polymerization of actin. Here we describe the cytoskeletal rearrangements during S. flexneri invasion of HeLa cells. After an initial contact of the bacterium with the cell surface, distinct nucleation zones of heavy chain actin polymerization appear in close proximity to the contact site underneath the parasite with long filaments being polymerized. These structures then push cellular protrusions that rise beside the entering bacterium, being sustained by tightly bundled long actin filaments organized in parallel orientation with their positive ends pointing to the cytoplasmic membrane. Finally, the cellular projections coalesce above the bacterial body, leading to its internalization. In addition, we found the actin-bundling protein plastin to be concentrated in these protrusions. Since plastin is known to bundle actin filaments in parallel orientation, colocalization of parallel actin filaments and plastin in the cellular protrusions strongly suggested a functional role of this protein in the architecture of parasite-induced cellular projections. Using transfection experiments, we show the differential recruitment of the two plastin isoforms (T- and L-) into Shigella entry zones. By transient expression of a truncated T-plastin which is deprived of one of its actin-binding sites, we also demonstrate the functional role of T-plastin in Shigella entry into HeLa cells.
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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.