ArticlePloS one2014
Host and bacterial proteins that repress recruitment of LC3 to Shigella early during infection.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Outer membrane vesicles secreted by avian pathogenic Escherichia coli promote its survival within macrophages and systemic infection by inducing endoplasmic reticulum stress-mediated autophagy flux blockade.Veterinary research · 2026Article
- Fighting the invader: strategies against intracellular bacteria.Frontiers in pharmacology · 2026Review
- Article
- Shigella flexneri evades LPS ubiquitylation through IpaH1.4-mediated degradation of RNF213.Nature structural & molecular biology · 2025Article
- Proximity biotinylation at the host-bioRxiv : the preprint server for biology · 2025Article
- Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024Article
- Molecular mechanisms of Shigella effector proteins: a common pathogen among diarrheic pediatric population.Molecular and cellular pediatrics · 2022Review
- The ubiquitin ligation machinery in the defense against bacterial pathogens.EMBO reports · 2021Review
- The Ubiquitination System within Bacterial Host-Pathogen Interactions.Microorganisms · 2021Review
- Review
- The T3SS ofMicroorganisms · 2020Review
- Article
- Eating the unknown: Xenophagy and ER-phagy are cytoprotective defenses against pathogens.Experimental cell research · 2020Review
- Review
- Actin Assembly around the Shigella-Containing Vacuole Promotes Successful Infection.Cell reports · 2020Article
- The Role of Autophagy and Autophagy Receptor NDP52 in Microbial Infections.International journal of molecular sciences · 2020Review
- Virulence-Related Gene Distribution AmongInfection and drug resistance · 2020Article
- Bacterial interaction with host autophagy.Virulence · 2019Review
- LC3-associated phagocytosis: host defense and microbial response.Current opinion in immunology · 2019Review
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 2 institutions in 1 country.
Funding
Abstract
Shigella spp. are intracytosolic gram-negative pathogens that cause disease by invasion and spread through the colonic mucosa, utilizing host cytoskeletal components to form propulsive actin tails. We have previously identified the host factor Toca-1 as being recruited to intracellular S. flexneri and being required for efficient bacterial actin tail formation. We show that at early times during infection (40 min.), the type three-secreted effector protein IcsB recruits Toca-1 to intracellular bacteria and that recruitment of Toca-1 is associated with repression of recruitment of LC3, as well as with repression of recruitment of the autophagy marker NDP52, around these intracellular bacteria. LC3 is best characterized as a marker of autophagosomes, but also marks phagosomal membranes in the process LC3-associated phagocytosis. IcsB has previously been demonstrated to be required for S. flexneri evasion of autophagy at late times during infection (4-6 hr) by inhibiting binding of the autophagy protein Atg5 to the Shigella surface protein IcsA (VirG). Our results suggest that IcsB and Toca-1 modulation of LC3 recruitment restricts LC3-associated phagocytosis and/or LC3 recruitment to vacuolar membrane remnants. Together with published results, our findings suggest that IcsB inhibits innate immune responses in two distinct ways, first, by inhibiting LC3-associated phagocytosis and/or LC3 recruitment to vacuolar membrane remnants early during infection, and second, by inhibiting autophagy late during infection.
Indexed as
Identifiers
What OpenQuestion holds
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.