Evidence map›Paper›PMID 10417179›Full record

ArticleInfection and immunity1999

Differential regulation of Salmonella typhimurium type III secreted proteins by pathogenicity island 1 (SPI-1)-encoded transcriptional activators InvF and hilA.

K Eichelberg, J E Galán

Abstract read
In one paragraph

Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

116 citing papers in PubMed.

  1. Article
  2. Oligomeric assembly of the gatekeeper InvE orchestrates hierarchical type III protein secretion inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. BCL2 regulates antibacterial autophagy in the intestinal epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Infection and immunity · 2024
    Article
  8. Detection ofAntibiotics (Basel, Switzerland) · 2024
    Article
  9. bioRxiv : the preprint server for biology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Harmine, an inhibitor of the type III secretion system ofFrontiers in cellular and infection microbiology · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Molecular Mechanisms ofInfection and drug resistance · 2020
    Review
  20. Article

56 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

K EichelbergSection of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale School of Medicine, New Haven, Connecticut 06536-0812, USA.
J E Galán

Funding

MOLECULAR GENETIC ANALYSIS OF SALMONELLA CELL INVASIONR37AI030492 · NIAID · YALE UNIVERSITY · PI GALAN, JORGE E · 2000 to 2024
$10.1M
MOLECULAR GENETIC ANALYSIS OF SALMONELLA CELL INVASIONR01AI030492 · NIAID · YALE UNIVERSITY · PI Jorge E Galan · 1995 to 2026
$3.1M
MOLECULAR GENETIC ANALYSIS OF SALMONELLA CELL INVASIONR29AI030492 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI GALAN, JORGE E · 1991 to 1995
–
NIAID NIH HHS AI30492NIAID NIH HHS R01 AI030492NIAID NIH HHS R37 AI030492
6 · The paper itself

Abstract

Salmonella enterica encodes a type III protein secretion system within a pathogenicity island (SPI-1) that is located at centisome 63 of its chromosome. This system is required for the ability of these bacteria to stimulate cellular responses that are essential for their pathogenicity. Expression of components and substrates of this system is subject to complex regulatory mechanisms. These mechanisms involve the function of HilA and InvF, two transcriptional regulatory proteins encoded within SPI-1. In this study, we examined the functional relationship between these two regulatory proteins. We found that strains carrying loss-of-function mutations in either hilA or invF differ in their ability to stimulate cellular responses. An S. typhimurium hilA mutant strain retained considerable signaling capacity that resulted in significant levels of internalization into host cells. In contrast, introduction of a nonpolar loss-of-function mutation in invF rendered S. typhimurium significantly impaired in its ability to enter host cells. Consistent with these different phenotypes, we found that HilA and InvF control the expression of different genes. HilA regulates the expression of components of the type III secretion machinery, whereas InvF controls the expression of type III secreted proteins encoded outside of SPI-1. We also found that the expression of secreted proteins encoded within SPI-1 are under the control of both HilA and InvF. Our results therefore indicate that InvF and HilA differentially control the expression of components and substrates of the invasion-associated type III secretion system.

Indexed as

DNA-Binding ProteinsFlagellinGene Expression Regulation, BacterialTranscription FactorsBacterial ProteinsCells, CulturedPromoter Regions, GeneticProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Salmonella typhimuriumSigma FactorTrans-ActivatorsBacterial ProteinsDNA-Binding ProteinsFlagellinFleB protein, Yersinia enterocoliticaHilA protein, SalmonellainvF protein, SalmonellaProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Sigma FactorTrans-ActivatorsTranscription Factors

Identifiers

PMID10417179
PMCPMC96710

What OpenQuestion holds

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Registered trials

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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.