Evidence map›Paper›PMID 9576950›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Activation of NF-kappaB via a Src-dependent Ras-MAPK-pp90rsk pathway is required for Pseudomonas aeruginosa-induced mucin overproduction in epithelial cells.

J D Li, W Feng, M Gallup, J H Kim, J Gum, Y Kim, C Basbaum

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
7.7field-weighted citation impact, top 2% of its field
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

98 citing papers in PubMed, 331 citations in OpenAlex.

  1. Frontiers in immunology · 2026
    Article
  2. Second-generation lysocins as therapeutics for treatingAntimicrobial agents and chemotherapy · 2025
    Article
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  12. Pseudomonas aeruginosa virulence proteins pseudolysin and protease IV impede cutaneous wound healing.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  13. Review
  14. Review
  15. Article
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  18. Article
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  20. Review

38 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

7 authors at 1 institution in 1 country.

J D LiDepartment of Anatomy, Program in Biomedical Sciences, and Cardiovascular Research Institute, University of California, San Francisco, CA 94143, USA.
W Feng
M Gallup
J H Kim
J Gum
Y Kim
C Basbaum
University of California, San Francisco · US

Funding

Tools for Analysis of Airway InflammationP01HL024136 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 1985 to 2014
$23.3M
NHLBI NIH HHS HL 24136NHLBI NIH HHS HL 43762
6 · The paper itself

Abstract

Cystic fibrosis (CF) is an autosomal recessive disorder, the most common lethal genetic disease in Caucasians. Respiratory disease is the major cause of morbidity and mortality. Indeed, 95% of CF patients die of respiratory failure. Pseudomonas aeruginosa, an opportunistic pathogen, chronically infects the lungs of over 85% of CF patients. It is ineradicable by antibiotics and responsible for airway mucus overproduction that contributes to airway obstruction and death. The molecular mechanisms underlying this pathology are unknown. Here we show that P. aeruginosa activates a c-Src-Ras-MEK1/2-MAPK-pp90rsk signaling pathway that leads to activation of nuclear factor NF-kappaB (p65/p50). Activated NF-kappaB binds to a kappaB site in the 5'-flanking region of the MUC2 gene and activates MUC2 mucin transcription. These studies bring new insight into bacterial-epithelial interactions and more specifically into the molecular pathogenesis of cystic fibrosis. Understanding these signaling and gene regulatory mechanisms opens up new therapeutic targets for cystic fibrosis.

Indexed as

Calcium-Calmodulin-Dependent Protein KinasesCells, CulturedCystic FibrosisEnzyme ActivationEpithelial CellsGenes, ReporterHumansLipopolysaccharidesLuciferasesModels, BiologicalMucinsNF-kappa BPromoter Regions, GeneticPseudomonas aeruginosaPseudomonas InfectionsRibosomal Protein S6 KinasesCalcium-Calmodulin-Dependent Protein KinasesLipopolysaccharidesLuciferasesMucinsNF-kappa BRibosomal Protein S6 Kinases

Identifiers

PMID9576950
PMCPMC20445
OpenAlexW2020191191

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.