Evidence map›Paper›PMID 9647642›Full record

ArticleThe Journal of cell biology1998

Suppression of steady-state, but not stimulus-induced NF-kappaB activity inhibits alphavirus-induced apoptosis.

K I Lin, J A DiDonato, A Hoffmann, J M Hardwick, R R Ratan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
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  9. Review
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  12. Inhibition of NF-kappa B activity and cFLIP expression contribute to viral-induced apoptosis.Apoptosis : an international journal on programmed cell death · 2005
    Article
  13. Article
  14. Article
  15. Nuclear factor-(kappa)B modulates the p53 response in neurons exposed to DNA damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  16. Review
  17. Sp1 and Sp3 are oxidative stress-inducible, antideath transcription factors in cortical neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  18. Article
  19. Growing old with nuclear factor-kappaB.Cell stress & chaperones · 2002
    Review
  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

5 authors at 3 institutions in 1 country.

K I LinDepartment of Molecular Microbiology and Immunology, The Johns Hopkins University School of Public Health, Baltimore, Maryland 21205, USA.
J A DiDonato
A Hoffmann
J M Hardwick
R R Ratan
Beth Israel Deaconess Medical Center · USMassachusetts Institute of Technology · USHarvard University · US

Funding

MECHANISMS OF PATHOLOGIC NEURONAL APOPTOSISK08NS001951 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI RATAN, RAJIV R · 1997 to 2001
$232k
NOVEL STRATEGIES TO LIMIT NEURONAL APOPTOSISR29NS034943 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI RATAN, RAJIV R · 1997 to 2001
$229k
NINDS NIH HHS KO8 NS01951NINDS NIH HHS R29 NS34943
6 · The paper itself

Abstract

Recent studies have established cell type- specific, proapoptotic, or antiapoptotic functions for the transcription factor NF-kappaB. In each of these studies, inhibitors of NF-kappaB activity have been present before the apoptotic stimulus, and so the role of stimulus- induced NF-kappaB activation in enhancing or inhibiting survival could not be directly assessed. Sindbis virus, an alphavirus, induces NF-kappaB activation and apoptosis in cultured cell lines. To address whether Sindbis virus- induced NF-kappaB activation is required for apoptosis, we used a chimeric Sindbis virus that expresses a superrepressor of NF-kappaB activity. Complete suppression of virus-induced NF-kappaB activity neither prevents nor potentiates Sindbis virus-induced apoptosis. In contrast, inhibition of NF-kappaB activity before infection inhibits Sindbis virus-induced apoptosis. Our results demonstrate that suppression of steady-state, but not stimulus-induced NF-kappaB activity, regulates expression of gene products required for Sindbis virus-induced death. Furthermore, we show that in the same cell line, NF-kappaB can be proapoptotic or antiapoptotic depending on the death stimulus. We propose that the role of NF-kappaB in regulating apoptosis is determined by the death stimulus and by the timing of modulating NF-kappaB activity relative to the death stimulus.

Indexed as

ApoptosisI-kappa B Proteins3T3 CellsAcetylcysteineAnimalsAntiviral AgentsDNA-Binding ProteinsGenetic VectorsHydrogen PeroxideMiceNF-kappa BNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitRatsSindbis VirusStaurosporineAcetylcysteineAntiviral AgentsDNA-Binding ProteinsHydrogen PeroxideI-kappa B ProteinsNF-kappa BNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitNfkbia protein, mouseNfkbia protein, ratStaurosporineTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID9647642
PMCPMC2133010
OpenAlexW1991900130

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.