Evidence map›Paper›PMID 26569329›Full record

ReviewBiomolecules2015

Transcriptional Activation of Inflammatory Genes: Mechanistic Insight into Selectivity and Diversity.

Afsar U Ahmed, Bryan R G Williams, Gregory E Hannigan

Abstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Effects of theInternational journal of molecular sciences · 2021
    Pooled it
  2. Trial
  3. Review
  4. Review
  5. Ebola virus matrix protein VP40 triggers inflammatory responses linked to the ebolavirus virulence.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Transcriptional control of ILC identity.Frontiers in immunology · 2023
    Review
  19. Article
  20. Article
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

3 authors.

Afsar U AhmedThe Centre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton VIC 3168, Australia. afsar.ahmed@hudson.org.au.
Bryan R G WilliamsThe Centre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton VIC 3168, Australia. bryan.williams@hudson.org.au.
Gregory E HanniganThe Centre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton VIC 3168, Australia. greg.hannigan@hudson.org.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute inflammation, an integral part of host defence and immunity, is a highly conserved cellular response to pathogens and other harmful stimuli. An inflammatory stimulation triggers transcriptional activation of selective pro-inflammatory genes that carry out specific functions such as anti-microbial activity or tissue healing. Based on the nature of inflammatory stimuli, an extensive exploitation of selective transcriptional activations of pro-inflammatory genes is performed by the host to ensure a defined inflammatory response. Inflammatory signal transductions are initiated by the recognition of inflammatory stimuli by transmembrane receptors, followed by the transmission of the signals to the nucleus for differential gene activations. The differential transcriptional activation of pro-inflammatory genes is precisely controlled by the selective binding of transcription factors to the promoters of these genes. Among a number of transcription factors identified to date, NF-κB still remains the most prominent and studied factor for its diverse range of selective transcriptional activities. Differential transcriptional activities of NF-κB are dictated by post-translational modifications, specificities in dimer formation, and variability in activation kinetics. Apart from the differential functions of transcription factors, the transcriptional activation of selective pro-inflammatory genes is also governed by chromatin structures, epigenetic markers, and other regulators as the field is continuously expanding.

Indexed as

AnimalsChemokinesChromatin Assembly and DisassemblyHumansInflammationMAP Kinase Signaling SystemNF-kappa BTranscriptional ActivationUbiquitinationChemokinesNF-kappa Bchromatin structuresepigenetic markersinflammationMAPKNF-κBnucleosome remodelingpro-inflammatory genestranscriptional activationubiquitination

Identifiers

PMID26569329
PMCPMC4693271

What OpenQuestion holds

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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.