ArticleTissue barriers2013
A bacterial encoded protein induces extreme multinucleation and cell-cell internalization in intestinal cells.
Article in Tissue barriers, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Alzheimer's Progenitor Amyloid-β Targets and Dissolves Microbial Amyloids and Impairs Biofilm Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- AnFrontiers in microbiology · 2021Article
- EnterohemorrhagicFrontiers in cell and developmental biology · 2020Article
- Clever Cooperation: Interactions Between EspF and Host Proteins.Frontiers in microbiology · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite extensive study, the molecular mechanisms that lead to multinucleation and cell enlargement (hypertrophy) remain poorly understood. Here, we show that a single bacterial virulence protein, EspF, from the human pathogen enteropathogenic E. coli induces extreme multi-nucleation in small intestinal epithelial cells. Ectopic expression of EspF induced cell-cell internalization events, presumably responsible for the enlarged multinucleated cells. These extreme phenotypes were dependent on a C-terminal polyproline-rich domain in EspF and not linked to the targeting of mitochondria or the nucleolus. The subversive functions of EspF may provide valuable insight into the molecular mechanisms that mediate cell fusion, multinucleation and cell hypertrophy.
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