ArticleCell adhesion & migration
Burkholderia cenocepacia infection: disruption of phagocyte immune functions through Rho GTPase inactivation.
Article in Cell adhesion & migration. 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, 6 citations in OpenAlex.
- Opsonization Improves Dual Proteomic Analysis ofJournal of proteome research · 2026Article
- Clostridioides difficile : A suspected pro-carcinogenic bacterium for gastrointestinal tumors.Chinese medical journal · 2026Review
- Lactobacillus spp. in the reproductive system of female moths and mating induced changes and possible transmission.BMC microbiology · 2022Article
- Control of Phagocytosis by Microbial Pathogens.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phagocytosis is an important component of innate immunity that contributes to the eradication of infectious microorganisms; however, successful bacterial pathogens often evade different aspects of host immune responses. A common bacterial evasion strategy entails the production of toxins and/or effectors that disrupt normal host cell processes and because of their importance Rho-family GTPases are often targeted. Burkholderia cenocepacia, an opportunistic pathogen that has a propensity to infect cystic fibrosis patients, is an example of a pathogenic bacterium that has only recently been shown to disrupt Rho GTPase function in professional phagocytes. More specifically, B. cenocepacia disrupts Rac and Cdc42 seemingly through perturbation of guanine nucleotide exchange factor function. Inactivation of Rac, Cdc42 and conceivably other Rho GTPases seriously compromises phagocyte function.
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Registered trials
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