ArticleInfection and immunity2013
The actin-polymerizing activity of SipA is not essential for Salmonella enterica serovar Typhimurium-induced mucosal inflammation.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Categorizing Sequences of Concern by Function To Better Assess Mechanisms of Microbial Pathogenesis.Infection and immunity · 2022Review
- Copper/Zinc-Modified Palygorskite Protects AgainstFrontiers in microbiology · 2021Article
- YshB Promotes Intracellular Replication and Is Required forJournal of bacteriology · 2019Article
- Minimal SPI1-T3SS effector requirement for Salmonella enterocyte invasion and intracellular proliferation in vivo.PLoS pathogens · 2018Article
- NOD1 and NOD2: Beyond Peptidoglycan Sensing.Trends in immunology · 2017Review
- InvS Coordinates Expression of PrgH and FimZ and Is Required for Invasion of Epithelial Cells by Salmonella enterica serovar Typhimurium.Journal of bacteriology · 2017Article
- Methods to Illuminate the Role ofFrontiers in cellular and infection microbiology · 2017Review
- Apical invasion of intestinal epithelial cells by Salmonella typhimurium requires villin to remodel the brush border actin cytoskeleton.Cell host & microbe · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Salmonella enterica serovar Typhimurium depends on type III secretion systems to inject effector proteins into host cells to promote bacterial invasion and to induce intestinal inflammation. SipA, a type III effector, is known to play important roles in both the invasion and the elicitation of intestinal inflammation. The actin-modulating activity of SipA has been shown to promote Salmonella entry into epithelial cells. To investigate whether the actin-modulating activity of SipA is required for its ability to induce an inflammatory response in vivo, we generated the SipA(K635A E637W) mutant, which is deficient in actin-modulating activity. Salmonella strains expressing the chromosomal SipA(K635A E637W) point mutation had reduced invasion abilities but still caused colitis similar to that caused by the wild-type strain in a mouse model of infection. Our data indicate that the SipA actin-polymerizing activity is not essential for the SipA-induced inflammatory response in the mouse model of 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.