Evidence map›Paper›PMID 8790359›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

Inhibition of cytokines and JAK-STAT activation by distinct signaling pathways.

T K Sengupta, E M Schmitt, L B Ivashkiv

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.9field-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

33 citing papers in PubMed, 134 citations in OpenAlex.

  1. Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
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  4. Review
  5. Article
  6. Macrophages as Emerging Key Players in Mitochondrial Transfers.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Zinc ameliorates intestinal barrier dysfunctions in shigellosis by reinstating claudin-2 and -4 on the membranes.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Article
  9. Article
  10. Review
  11. Article
  12. Galectin-1 promotes an M2 macrophage response to polydioxanone scaffolds.Journal of biomedical materials research. Part A · 2017
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cytokines: Names and Numbers You Should Care About.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Review
  19. Article
  20. Review
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 at 2 institutions in 1 country.

T K SenguptaDepartment of Medicine, Hospital for Special Surgery, New York, NY 10021, USA.
E M Schmitt
L B Ivashkiv
Hospital for Special Surgery · USCornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An important component of cytokine regulation of cell growth and differentiation is rapid transcriptional activation of genes by the JAK-STAT (signal transducer and activator of transcription) signaling pathway. Ligation of cytokine receptors results in tyrosine phosphorylation and activation of receptor-associated Jak protein tyrosine kinases and cytoplasmic STAT transcription factors, which then translocate to the nucleus. We describe the interruption of cytokine triggered JAK-STAT signals by cAMP, the calcium ionophore ionomycin, and granulocyte/macrophage colony-stimulating factor. Jak1 kinase activity, interleukin 6-induced gene activation, Stat3 tyrosine phosphorylation, and DNA-binding were inhibited, as was activation of Jak1 and Stat1 by interferon gamma. The kinetics and requirement for new RNA and protein synthesis for inhibition of interleukin 6 by ionomycin and GM-CSF differed, but both agents increased the association of Jak1 with protein tyrosine phosphatase ID (SH2-containing phosphatase 2). Our results demonstrate that crosstalk with distinct signaling pathways can inhibit JAK-STAT signal transduction, and suggest approaches for modulating cytokine activity during immune responses and inflammatory processes.

Indexed as

Signal TransductionTranscription, GeneticBlotting, NorthernCells, CulturedCyclic AMPCycloheximideCytokinesDactinomycinDNADNA-Binding ProteinsEnzyme ActivationGranulocyte-Macrophage Colony-Stimulating FactorHumansInterferon-gammaInterleukin-6 InhibitorsIntracellular Signaling Peptides and ProteinsCyclic AMPCycloheximideCytokinesDactinomycinDNADNA-Binding ProteinsGranulocyte-Macrophage Colony-Stimulating FactorInterferon-gammaInterleukin-6 InhibitorsIntracellular Signaling Peptides and ProteinsIonomycinJAK1 protein, humanJAK3 protein, humanJanus Kinase 1Janus Kinase 3Protein Phosphatase 2Protein-Tyrosine KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPTPN11 protein, humanPTPN6 protein, humanRNASTAT1 protein, humanSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorTrans-Activators

Identifiers

PMID8790359
PMCPMC38457
OpenAlexW1983453744

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.