Evidence map›Paper›PMID 20587593›Full record

ArticleJournal of cell science2010

Co-regulation of nuclear respiratory factor-1 by NFkappaB and CREB links LPS-induced inflammation to mitochondrial biogenesis.

Hagir B Suliman, Timothy E Sweeney, Crystal M Withers, Claude A Piantadosi

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.0field-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

49 citing papers in PubMed, 105 citations in OpenAlex.

  1. CREB regulates Foxp3Frontiers in immunology · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Testosterone attenuates hypoxia-induced hypertension by affecting NRF1-mediated transcriptional regulation of ET-1 and ACE.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. miR‑146a improves hepatic lipid and glucose metabolism by targeting MED1.International journal of molecular medicine · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

4 authors at 2 institutions in 1 country.

Hagir B SulimanDepartment of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA.
Timothy E Sweeney
Crystal M Withers
Claude A Piantadosi
Duke University Hospital · USDuke Medical Center · US

Funding

Regulation of mitochondrial biogenesis by heme oxygenase-1R01HL090679 · NHLBI · DUKE UNIVERSITY · PI PIANTADOSI, CLAUDE A · 2008 to 2011
$1.6M
NHLBI NIH HHS R01 HL090679NIAID NIH HHS R01 AI0664789
6 · The paper itself

Abstract

The nuclear respiratory factor-1 (NRF1) gene is activated by lipopolysaccharide (LPS), which might reflect TLR4-mediated mitigation of cellular inflammatory damage via initiation of mitochondrial biogenesis. To test this hypothesis, we examined NRF1 promoter regulation by NFκB, and identified interspecies-conserved κB-responsive promoter and intronic elements in the NRF1 locus. In mice, activation of Nrf1 and its downstream target, Tfam, by Escherichia coli was contingent on NFκB, and in LPS-treated hepatocytes, NFκB served as an NRF1 enhancer element in conjunction with NFκB promoter binding. Unexpectedly, optimal NRF1 promoter activity after LPS also required binding by the energy-state-dependent transcription factor CREB. EMSA and ChIP assays confirmed p65 and CREB binding to the NRF1 promoter and p65 binding to intron 1. Functionality for both transcription factors was validated by gene-knockdown studies. LPS regulation of NRF1 led to mtDNA-encoded gene expression and expansion of mtDNA copy number. In cells expressing plasmid constructs containing the NRF-1 promoter and GFP, LPS-dependent reporter activity was abolished by cis-acting κB-element mutations, and nuclear accumulation of NFκB and CREB demonstrated dependence on mitochondrial H(2)O(2). These findings indicate that TLR4-dependent NFκB and CREB activation co-regulate the NRF1 promoter with NFκB intronic enhancement and redox-regulated nuclear translocation, leading to downstream target-gene expression, and identify NRF-1 as an early-phase component of the host antibacterial defenses.

Indexed as

AnimalsChromatin ImmunoprecipitationComputational BiologyCyclic AMP Response Element-Binding ProteinDNA, MitochondrialElectrophoretic Mobility Shift AssayHep G2 CellsHumansImmunoblottingInflammationIntronsLipopolysaccharidesMaleMiceMice, Inbred C57BLMitochondria3-(4-methylphenylsulfonyl)-2-propenenitrileCyclic AMP Response Element-Binding ProteinDNA, MitochondrialLipopolysaccharidesNF-kappa BNitrilesNuclear Respiratory Factor 1Sulfones

Identifiers

PMID20587593
PMCPMC2912462
OpenAlexW2142063052

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.