ArticleCellular microbiology2013
Induction of caspase 3 activation by multiple Legionella pneumophila Dot/Icm substrates.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Legionella effector LpPIP recruits protein phosphatase 1 to the mitochondria to induce dephosphorylation of outer membrane proteins.PLoS biology · 2025Article
- The bacterial effector SidN/Lpg1083 promotes cell death by targeting Lamin-B2.Journal of molecular cell biology · 2023Article
- Non-Canonical Inflammasome Pathway: The Role of Cell Death and Inflammation in Ehrlichiosis.Cells · 2023Review
- TNF-α response in macrophages depends on clinicalVirulence · 2022Article
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- Comparative Lipidomic Analysis of Extracellular Vesicles Derived fromInternational journal of molecular sciences · 2020Article
- Genomic Analysis of Wolbachia from Laodelphax striatellus (Delphacidae, Hemiptera) Reveals Insights into Its "Jekyll and Hyde" Mode of Infection Pattern.Genome biology and evolution · 2020Article
- Phosphoinositides and the Fate ofFrontiers in immunology · 2020Review
- Viewing Legionella pneumophila Pathogenesis through an Immunological Lens.Journal of molecular biology · 2019Review
- Stenotrophomonas maltophilia Encodes a VirB/VirD4 Type IV Secretion System That Modulates Apoptosis in Human Cells and Promotes Competition against Heterologous Bacteria, Including Pseudomonas aeruginosa.Infection and immunity · 2019Article
- Evasion of phagotrophic predation by protist hosts and innate immunity of metazoan hosts by Legionella pneumophila.Cellular microbiology · 2019Review
- Differential expression of virulence genes in Legionella pneumophila growing in Acanthamoeba and human monocytes.Virulence · 2018Article
- Article
- Patatin-like phospholipases in microbial infections with emerging roles in fatty acid metabolism and immune regulation by Apicomplexa.Molecular microbiology · 2018Review
- Legionella and Coxiella effectors: strength in diversity and activity.Nature reviews. Microbiology · 2017Review
- The Toolbox for Uncovering the Functions ofFrontiers in cellular and infection microbiology · 2017Review
- A Legionella Effector Disrupts Host Cytoskeletal Structure by Cleaving Actin.PLoS pathogens · 2017Article
- Article
- Caspase Exploitation by Legionella pneumophila.Frontiers in microbiology · 2016Review
- A novel phosphatidylinositol 4,5-bisphosphate binding domain mediates plasma membrane localization of ExoU and other patatin-like phospholipases.The Journal of biological chemistry · 2015Article
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 3 institutions in 1 country.
Funding
Abstract
The intracellular pathogen Legionella pneumophila is able to strike a balance between the death and survival of the host cell during infection. Despite the presence of high level of active caspase 3, the executioner caspase of apoptotic cell death, infected permissive macrophages are markedly resistant to exogenous apoptotic stimuli. Several bacterial molecules capable of promoting the cell survival pathways have been identified, but proteins involved in the activation of caspase 3 remain unknown. To study the mechanism of L. pneumophila-mediated caspase 3 activation, we tested all known Dot/Icm substrates for their ability to activate caspase 3. Five effectors capable of causing caspase 3 activation upon transient expression were identified. Among these, by using its ability to activate caspase 3 by inducing the release of cytochrome c from the mitochondria, we demonstrated that VipD is a phospholipase A2, which hydrolyses phosphatidylethanolamine (PE) and phosphocholine (PC) on the mitochondrial membrane in a manner that appears to require host cofactor(s). The lipase activity leads to the production of free fatty acids and 2-lysophospholipids, which destabilize the mitochondrial membrane and may contribute to the release of cytochrome c and the subsequent caspase 3 activation. Furthermore, we found that whereas it is not detectably defectively in caspase 3 activation in permissive cells, amutant lacking all of these five genes is less potent in inducing apoptosis in dendritic cells. Our results reveal that activation of host cell death pathways by L. pneumophila is a result of the effects of multiple bacterial proteins with diverse biochemical functions.
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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.