Evidence map›Paper›PMID 19800126›Full record

ArticleMolecular immunology2009

Catalytic activity of the proteasome fine-tunes Brg1-mediated chromatin remodeling to regulate the expression of inflammatory genes.

Sarah J Cullen, Subramaniam Ponnappan, Usha Ponnappan

Abstract read
In one paragraph

Article in Molecular immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. LP99: Discovery and Synthesis of the First Selective BRD7/9 Bromodomain Inhibitor.Angewandte Chemie (International ed. in English) · 2015
    Article
  6. LP99: Discovery and Synthesis of the First Selective BRD7/9 Bromodomain Inhibitor.Angewandte Chemie (Weinheim an der Bergstrasse, Germany) · 2015
    Article
  7. Review
  8. Article
  9. Review
  10. Bromodomains as therapeutic targets.Expert reviews in molecular medicine · 2011
    Review
  11. 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 1 institution in 1 country.

Sarah J CullenDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Subramaniam Ponnappan
Usha Ponnappan
University of Arkansas for Medical Sciences · US

Funding

Modulation of Immune senescence by induction of Ubiquitin-Proteasome systemsR01AG030599 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI PONNAPPAN, USHA · 2008 to 2012
$1.3M
Regulatory Ubiquitination in Immune senescenceR01AG025220 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI PONNAPPAN, USHA · 2007 to 2011
$1.2M
TRANSCRIPTION FACTOR NFKB AND IMMUNE SENESCENCER01AG013081 · NIA · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI PONNAPPAN, USHA · 1996 to 2004
$992k
NIA NIH HHS AG025220NIA NIH HHS AG030599NIA NIH HHS AG13081NIA NIH HHS R01 AG013081NIA NIH HHS R01 AG025220NIA NIH HHS R01 AG030599
6 · The paper itself

Abstract

The induction of key pro-inflammatory genes is regulated by the SWI/SNF class of ATP-dependent remodeling complexes. In particular, the catalytic ATPase subunit, Brg1, is distinctly involved in the chromatin remodeling required for activating pro-inflammatory genes in a temporally, ordered fashion. Despite advances in our understanding of the role for Brg1 in the kinetics of inflammatory responses, little is known about the precise mechanisms which down-regulate Brg1 activity. Biochemical studies implicate a role for the proteasome in the regulation of SWI/SNF assembly and function; however, it is unclear if proteasome-dependent mechanisms modulate its remodeling activity or recruitment to chromatin in order to regulate inflammatory gene transcription. We now demonstrate for the first time that proteasome function represents an important mechanism for limiting inducible association of Brg1 with promoters of SWI/SNF-regulated, inflammatory genes. As a result, catalytic activity of the proteasome fine-tunes the kinetics of inflammatory gene transcription by inhibiting both premature and persistent chromatin remodeling at SWI/SNF-regulated genes. These results provide mechanistic insight into the interplay between nucleosome remodeling, inflammation and proteasome, and underscore the critical role of the proteasome in controlling both extent and duration of inflammatory responses.

Indexed as

BiocatalysisAclarubicinAnimalsChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDNA HelicasesInflammationInterleukin-6KineticsMiceNuclear ProteinsNucleosomesPromoter Regions, GeneticProteasome Endopeptidase ComplexProteasome InhibitorsTranscription FactorsaclacinomycinsAclarubicinChromosomal Proteins, Non-HistoneDNA HelicasesInterleukin-6Nuclear ProteinsNucleosomespervanadateProteasome Endopeptidase ComplexProteasome InhibitorsSmarca4 protein, mouseSWI-SNF-B chromatin-remodeling complexTranscription FactorsVanadates

Identifiers

PMID19800126
PMCPMC2788002
OpenAlexW1986404100

What OpenQuestion holds

Textmetadata
LicenceTDM
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.