ReviewFrontiers in cellular and infection microbiology2016
How Shigella Utilizes Ca(2+) Jagged Edge Signals during Invasion of Epithelial Cells.
Review in Frontiers in cellular and infection microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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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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
13 citing papers in PubMed, 26 citations in OpenAlex.
- Detection of Calpain-Mediated Beclin-1 Cleavage for Drug Discovery in Inflammatory Bowel Diseases.Cells · 2026Article
- The host calcium system contributes to intracellularInfection and immunity · 2025Article
- Nicotine's impact on platelet function: insights into hemostasis mechanisms.Frontiers in pharmacology · 2024Article
- Molecular mechanisms of Shigella effector proteins: a common pathogen among diarrheic pediatric population.Molecular and cellular pediatrics · 2022Review
- Reprogramming of Cell Death Pathways by Bacterial Effectors as a Widespread Virulence Strategy.Infection and immunity · 2022Review
- Contribution of large-pore channels to inflammation induced by microorganisms.Frontiers in cell and developmental biology · 2022Review
- Article
- Calcium-sensing receptor deletion in the mouse esophagus alters barrier function.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Article
- Review
- How Viral and Intracellular Bacterial Pathogens Reprogram the Metabolism of Host Cells to Allow Their Intracellular Replication.Frontiers in cellular and infection microbiology · 2019Review
- Article
- Fine tuning of cytosolic Ca (2+) oscillations.F1000Research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shigella, the causative agent of bacillary dysentery invades intestinal epithelial cells using a type III secretion system (T3SS). Through the injection of type III effectors, Shigella manipulates the actin cytoskeleton to induce its internalization in epithelial cells. At early invasion stages, Shigella induces atypical Ca(2+) responses confined at entry sites allowing local cytoskeletal remodeling for bacteria engulfment. Global Ca(2+) increase in the cell triggers the opening of connexin hemichannels at the plasma membrane that releases ATP in the extracellular milieu, favoring Shigella invasion and spreading through purinergic receptor signaling. During intracellular replication, Shigella regulates inflammatory and death pathways to disseminate within the epithelium. At later stages of infection, Shigella downregulates hemichannel opening and the release of extracellular ATP to dampen inflammatory signals. To avoid premature cell death, Shigella activates cell survival by upregulating the PI3K/Akt pathway and downregulating the levels of p53. Furthermore, Shigella interferes with pro-apoptotic caspases, and orients infected cells toward a slow necrotic cell death linked to mitochondrial Ca(2+) overload. In this review, we will focus on the role of Ca(2+) responses and their regulation by Shigella during the different stages of bacterial infection.
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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.