Evidence map›Paper›PMID 8497250›Full record

ArticleMolecular and cellular biology1993

The response of gamma interferon activation factor is under developmental control in cells of the macrophage lineage.

A Eilers, D Seegert, C Schindler, M Baccarini, T Decker

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Inteferons pen the JAK-STAT pathway.Seminars in cell & developmental biology · 2008
    Review
  5. Article
  6. Article
  7. Article
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  16. Article
  17. Macrophage nitric oxide synthase gene: two upstream regions mediate induction by interferon gamma and lipopolysaccharide.Proceedings of the National Academy of Sciences of the United States of America · 1993
    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

5 authors at 1 institution in 1 country.

A EilersFraunhofer Institute for Toxicology and Molecular Biology, Hannover, Germany.
D Seegert
C Schindler
M Baccarini
T Decker
Fraunhofer Institute for Toxicology and Experimental Medicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gamma interferon activation factor (GAF) rapidly induces transcriptional activation of gamma interferon (IFN-gamma)-responsive genes. Conversion of the GAF from a latent cytoplasmic to an activated, DNA-binding form is an immediate step in the cellular response to IFN-gamma. The amount of IFN-gamma-activated GAF, measured by exonuclease III protection or gel shift assays, increased strongly upon monocytic differentiation of U937 cells. Activated GAF contained the IFN-responsive 91-kDa protein as its DNA-binding activity in gel shift or exonuclease III assays could be inhibited through direct addition of specific antiserum, and it was not present in p91-immunodepleted extracts. There was a differentiation-induced increase in the amount of nonphosphorylated (latent) p91. Transcription rate measurement demonstrated a strong induction of the p91 gene during monocytic differentiation of U937 cells. The amount of p91 which was rapidly phosphorylated in response to IFN-gamma was found to be much higher in the differentiated cells and suggested a differentiation-controlled increase in the signaling leading to p91 phosphorylation. Concomitantly with a better GAF response, transcriptional activation of IFN-gamma-induced genes and the expression of GAF-dependent, transfected reporter plasmids increased in differentiated U937 monocytes. The promonocyte-monocyte transition also affected the IFN-alpha-responsive transcription factor ISGF-3. Differentiated U937 cells contained more of both the alpha-component p91 and the gamma-component p48, which constitutes the DNA-binding subunit of the complex. Our study thus provides evidence that the synthesis of specific transcription factors can be a regulated event to control the cytokine responsiveness of cells during development.

Indexed as

Binding SitesCell DifferentiationCell NucleusChloramphenicol O-AcetyltransferaseCytoplasmExodeoxyribonucleasesHeLa CellsHumansInterferon-gammaInterferon-Stimulated Gene Factor 3Macromolecular SubstancesMacrophagesPhosphoproteinsPhosphorylationTetradecanoylphorbol AcetateTranscription FactorsChloramphenicol O-Acetyltransferaseexodeoxyribonuclease IIIExodeoxyribonucleasesgamma interferon activation factorInterferon-gammaInterferon-Stimulated Gene Factor 3Macromolecular SubstancesPhosphoproteinsTetradecanoylphorbol AcetateTranscription Factors

Identifiers

PMID8497250
PMCPMC359771
OpenAlexW1861818061

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.