ArticleCellular microbiology2010
The bacterial effectors EspG and EspG2 induce a destructive calpain activity that is kept in check by the co-delivered Tir effector.
Article in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- A comprehensive two-hybrid analysis to explore themSystems · 2024Article
- EnteropathogenicMicroorganisms · 2024Article
- Enterohaemorrhagic E. coli modulates an ARF6:Rab35 signaling axis to prevent recycling endosome maturation during infection.Journal of molecular biology · 2016Article
- Trypanosoma cruzi Differentiates and Multiplies within Chimeric Parasitophorous Vacuoles in Macrophages Coinfected with Leishmania amazonensis.Infection and immunity · 2016Article
- Modulation of p53 during bacterial infections.Nature reviews. Microbiology · 2015Review
- Calpain-dependent cytoskeletal rearrangement exploited for anthrax toxin endocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Pathogenesis of human enterovirulent bacteria: lessons from cultured, fully differentiated human colon cancer cell lines.Microbiology and molecular biology reviews : MMBR · 2013Review
- A bacterial encoded protein induces extreme multinucleation and cell-cell internalization in intestinal cells.Tissue barriers · 2013Article
- Insights into the pathogenesis of enteropathogenic E. coli using an improved intestinal enterocyte model.PloS one · 2013Article
- The enteropathogenic E. coli (EPEC) Tir effector inhibits NF-κB activity by targeting TNFα receptor-associated factors.PLoS pathogens · 2011Article
- Calpain mediates epithelial cell microvillar effacement by enterohemorrhagic Escherichia coli.Frontiers in microbiology · 2011Article
- The EspF effector, a bacterial pathogen's Swiss army knife.Infection and immunity · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Bacterial pathogens deliver multiple effector proteins into eukaryotic cells to subvert host cellular processes and an emerging theme is the cooperation between different effectors. Here, we reveal that a fine balance exists between effectors that are delivered by enteropathogenic E. coli (EPEC) which, if perturbed can have marked consequences on the outcome of the infection. We show that absence of the EPEC effector Tir confers onto the bacterium a potent ability to destroy polarized intestinal epithelia through extensive host cell detachment. This process was dependent on the EPEC effectors EspG and EspG2 through their activation of the host cysteine protease calpain. EspG and EspG2 are shown to activate calpain during EPEC infection, which increases significantly in the absence of Tir - leading to rapid host cell loss and necrosis. These findings reveal a new function for EspG and EspG2 and show that Tir, independent of its bacterial ligand Intimin, is essential for maintaining the integrity of the epithelium during EPEC infection by keeping the destructive activity of EspG and EspG2 in check.
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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.