ArticleInfection and immunity2009
The enteropathogenic Escherichia coli effector Cif induces delayed apoptosis in epithelial cells.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 68 citations in OpenAlex.
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- Shiga toxin-producing Escherichia coli plasmid diversity reveals virulence potential and control opportunities in animal hosts.Scientific reports · 2025Article
- EnterohemorrhagicInfection and immunity · 2024Article
- Impact of enteric bacterial infections at and beyond the epithelial barrier.Nature reviews. Microbiology · 2023Review
- Breaking bad: necroptosis in the pathogenesis of gastrointestinal diseases.Frontiers in immunology · 2023Review
- The transmembrane domains of the type III secretion system effector Tir are involved in its secretion and cellular activities.Frontiers in cellular and infection microbiology · 2023Article
- Phenotyping of Fecal Microbiota of Winnie, a Rodent Model of Spontaneous Chronic Colitis, Reveals Specific Metabolic, Genotoxic, and Pro-inflammatory Properties.Inflammation · 2022Article
- Host Genetics and Microbiota Interactions in Colorectal Cancer: Shared or Independent Risk?Microorganisms · 2022Review
- The Role of Cyclomodulins and Some Microbial Metabolites in Bacterial Microecology and Macroorganism Carcinogenesis.International journal of molecular sciences · 2022Review
- Cycle-Inhibiting Factor Is Associated withBiology · 2022Article
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- Reprogramming of Cell Death Pathways by Bacterial Effectors as a Widespread Virulence Strategy.Infection and immunity · 2022Review
- Map of EnteropathogenicInternational journal of molecular sciences · 2022Article
- Which bacterial toxins are worthy of validation as markers in colorectal cancer screening? A critical review.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2022Review
- Mitotic Arrest-Deficient 2 Like 2 (MAD2L2) Interacts withLife (Basel, Switzerland) · 2021Article
- The Role of the Gut Microbiota in Colorectal Cancer Causation.International journal of molecular sciences · 2019Review
- Shiga toxin sub-type 2a increases the efficiency of Escherichia coli O157 transmission between animals and restricts epithelial regeneration in bovine enteroids.PLoS pathogens · 2019Article
- Post-translational regulation of ubiquitin signaling.The Journal of cell biology · 2019Review
- Heterogeneous Family of Cyclomodulins: Smart Weapons That Allow Bacteria to Hijack the Eukaryotic Cell Cycle and Promote Infections.Frontiers in cellular and infection microbiology · 2017Review
- Article
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
No grant is acknowledged in the PubMed record.
Abstract
The cycle inhibiting factor (Cif) belongs to a family of bacterial toxins, the cyclomodulins, which modulate the host cell cycle. Upon injection into the host cell by the type III secretion system of enteropathogenic Escherichia coli (EPEC), Cif induces both G(2) and G(1) cell cycle arrests. The cell cycle arrests correlate with the accumulation of p21(waf1) and p27(kip1) proteins that inhibit CDK-cyclin complexes, whose activation is required for G(1)/S and G(2)/M transitions. Increases of p21 and p27 levels are independent of p53 transcriptional induction and result from protein stabilization through inhibition of the ubiquitin/proteasome degradation pathway. In this study, we show that Cif not only induces cell cycle arrest but also eventually provokes a delayed cell death. Indeed, 48 h after infection with EPEC expressing Cif, cultured IEC-6 intestinal cells were positive for extracellular binding of annexin V and exhibited high levels of cleaved caspase-3 and lactate dehydrogenase release, indicating evidence of apoptosis. Cif was necessary and sufficient for inducing this late apoptosis, and the cysteine residue of the catalytic site was required for Cif activity. These results highlight a more complex role of Cif than previously thought, as a cyclomodulin but also as an apoptosis inducer.
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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.