Evidence map›Paper›PMID 10848596›Full record

ArticleMolecular and cellular biology2000

Peroxisome proliferator-activated receptor gamma-dependent repression of the inducible nitric oxide synthase gene.

M Li, G Pascual, C K Glass

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 369 citations in OpenAlex.

  1. Article
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  5. Matrix Metalloproteinase-9 Signaling Regulates Colon Barrier Integrity in Models of HIV Infection.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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  8. Article
  9. Article
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  18. Protein Lipoxidation: Basic Concepts and Emerging Roles.Antioxidants (Basel, Switzerland) · 2021
    Review
  19. Review
  20. Review

68 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

3 authors at 1 institution in 1 country.

M LiDepartment of Cellular and Molecular Medicine, University of California, San Diego, La Jolla 92093-0651, USA.
G Pascual
C K Glass
University of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The peroxisome proliferator-activated receptor gamma (PPARgamma) is a member of the nuclear receptor superfamily that activates target gene transcription in a ligand-dependent manner. In addition, liganded PPARgamma can inhibit transcription of genes induced by gamma interferon (IFN-gamma) and/or lipopolysaccharides (LPSs), including the inducible nitric oxide synthase (iNOS) gene. Inhibition of the iNOS promoter is achieved partially through antagonizing the activities of NF-kappaB, AP-1, and STAT1, which are known to mediate effects of LPS and IFN-gamma. Previous studies have suggested that transrepression of these factors by nuclear receptors involves competition for limiting amounts of the general coactivators CREB-binding protein (CBP) and p300. CBP and p300 are thought to be recruited to nuclear receptors through bridging factors that include SRC-1, although CBP also interacts directly with PPARgamma through its amino terminus. These observations have raised questions concerning the involvement of SRC-1-like factors in CBP recruitment and transrepression. We here provide evidence that PPARgamma's ability to repress iNOS transcription requires the ligand-dependent charge clamp that mediates interactions with CBP and SRC-1. Single amino acid mutations in PPARgamma that abolished ligand-dependent interactions with SRC-1 and CBP not only resulted in complete loss of transactivation activity but also abolished transrepression. Conversely, a CBP deletion mutant containing the SRC-1 interaction domain but lacking the N-terminal PPARgamma interaction domain was inactive as a PPARgamma coactivator and failed to rescue transrepression. Together, these findings are consistent with a model in which transrepression by PPARgamma is achieved by targeting CBP through direct interaction with its N-terminal domain and via SRC-1-like bridge factors.

Indexed as

ThiazolidinedionesAnimalsBinding SitesCREB-Binding ProteinDimerizationDNA-Binding ProteinsGene Expression RegulationHistone AcetyltransferasesMacrophagesMiceMutationNitric Oxide SynthaseNitric Oxide Synthase Type IINuclear ProteinsNuclear Receptor Coactivator 1PhosphorylationCREB-Binding ProteinCrebbp protein, mouseDNA-Binding ProteinsHistone AcetyltransferasesNcoa1 protein, mouseNitric Oxide SynthaseNitric Oxide Synthase Type IINos2 protein, mouseNuclear ProteinsNuclear Receptor Coactivator 1Receptors, Cytoplasmic and NuclearRecombinant ProteinsRosiglitazoneThiazolesThiazolidinedionesTrans-ActivatorsTranscription Factors

Identifiers

PMID10848596
PMCPMC85890
OpenAlexW2133941138

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.