Evidence map›Paper›PMID 15024088›Full record

ArticleMolecular and cellular biology2004

HBP1 repression of the p47phox gene: cell cycle regulation via the NADPH oxidase.

Stephen P Berasi, Mei Xiu, Amy S Yee, K Eric Paulson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

34 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. HBP1-mediated transcriptional repression of AFP inhibits hepatoma progression.Journal of experimental & clinical cancer research : CR · 2021
    Article
  7. miR-335-5P contributes to human osteoarthritis by targeting HBP1.Experimental and therapeutic medicine · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Regulation of NADPH oxidases in skeletal muscle.Free radical biology & medicine · 2016
    Review
  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.

Stephen P BerasiDepartment of Biochemistry, Tufts University School of Medicine, School of Nutrition, Boston, Massachusetts 02111, USA.
Mei Xiu
Amy S Yee
K Eric Paulson
Tufts University · USTufts Medical Center · US

Funding

PILOT AND FEASIBILITY STUDIESP30DK034928 · NIDDK · TUFTS MEDICAL CENTER · PI PLAUT, ANDREW GEORGE · 1986 to 2007
$8.5M
Mechanisms of Transcriptional Repressor HBP1 in CancerR01CA094187 · NCI · TUFTS UNIVERSITY BOSTON · PI YEE, AMY S. · 2002 to 2006
$1.4M
TRANSCRIPTIONAL REPRESSION AND CELL CYCLE MECHANISMSR01GM044634 · NIGMS · TUFTS UNIVERSITY BOSTON · PI YEE, AMY S. · 1991 to 2000
$363k
p38 MAP Kinase/HBP1 Regulation of Reactive Oxygen Speci*R03ES011518 · NIEHS · TUFTS UNIVERSITY BOSTON · PI PAULSON, KURTZ ERIC · 2001 to 2002
$159k
NCI NIH HHS R01 CA094187NIDDK NIH HHS P30 DK034928NIDDK NIH HHS P30 DK34928NIEHS NIH HHS ES11518NIGMS NIH HHS GM44634
6 · The paper itself

Abstract

Several studies have linked the production of reactive oxygen species (ROS) by the NADPH oxidase to cellular growth control. In many cases, activation of the NADPH oxidase and subsequent ROS generation is required for growth factor signaling and mitogenesis in nonimmune cells. In this study, we demonstrate that the transcriptional repressor HBP1 (HMG box-containing protein 1) regulates the gene for the p47phox regulatory subunit of the NADPH oxidase. HBP1 represses growth regulatory genes (e.g., N-Myc, c-Myc, and cyclin D1) and is an inhibitor of G(1) progression. The promoter of the p47phox gene contains six tandem high-affinity HBP1 DNA-binding elements at positions -1243 to -1318 bp from the transcriptional start site which were required for repression. Furthermore, HBP1 repressed the expression of the endogenous p47phox gene through sequence-specific binding. With HBP1 expression and the subsequent reduction in p47phox gene expression, intracellular superoxide production was correspondingly reduced. Using both the wild type and a dominant-negative mutant of HBP1, we demonstrated that the repression of superoxide production through the NADPH oxidase contributed to the observed cell cycle inhibition by HBP1. Together, these results indicate that HBP1 may contribute to the regulation of NADPH oxidase-dependent superoxide production through transcriptional repression of the p47phox gene. This study defines a transcriptional mechanism for regulating intracellular ROS levels and has implications in cell cycle regulation.

Indexed as

Gene Expression RegulationAnimalsCell CycleCell LineHigh Mobility Group ProteinsHumansMiceModels, BiologicalNADPH OxidasesPhosphoproteinsPromoter Regions, GeneticReactive Oxygen SpeciesRepressor ProteinsSuperoxidesHBP1 protein, humanHbp1 protein, mouseHigh Mobility Group ProteinsNADPH Oxidasesneutrophil cytosolic factor 1PhosphoproteinsReactive Oxygen SpeciesRepressor ProteinsSuperoxides

Identifiers

PMID15024088
PMCPMC371097
OpenAlexW2126708302

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.