Evidence map›Paper›PMID 19450264›Full record

ReviewJournal of neuroinflammation2009

Unique aspects of transcriptional regulation in neurons--nuances in NFkappaB and Sp1-related factors.

Xianrong R Mao, Andréa M Moerman-Herzog, Yuzhi Chen, Steven W Barger

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Alcohol, HMGB1, and Innate Immune Signaling in the Brain.Alcohol research : current reviews · 2024
    Review
  4. βIII-Tubulin Gene Regulation in Health and Disease.Frontiers in cell and developmental biology · 2022
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Screening of Potential Genes and Transcription Factors of Postoperative Cognitive Dysfunction via Bioinformatics Methods.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  12. Review
  13. Maternal IL-17A in autism.Experimental neurology · 2018
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  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 3 institutions in 1 country.

Xianrong R MaoDepartment of Anesthesiology, Washington University School of Medicine, St Louis, MO 63110, USA. maox@morpheus.wustl.edu
Andréa M Moerman-Herzog
Yuzhi Chen
Steven W Barger
University of Arkansas for Medical Sciences · USCentral Arkansas Veterans Healthcare System · USWashington University in St. Louis · US

Funding

THE APOE-APP AXIS IN ALZHEIMER PATHOGENESISP01AG012411 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI GRIFFIN, SUE TILTON · 1995 to 2020
$25.0M
Sp1, kappa-B enhancers and transcriptions in neuronsR01NS046439 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI BARGER, STEVEN W · 2004 to 2009
$1.3M
Amyloid Precursor Protein and UbiquitinationR01AG034980 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI CHEN, YUZHI · 2010 to 2014
$997k
NIA NIH HHS P01 AG012411NIA NIH HHS P01AG12411NIA NIH HHS R01 AG034980NINDS NIH HHS R01 NS046439NINDS NIH HHS R01NS046439
6 · The paper itself

Abstract

The unique physiology and function of neurons create differences in their cellular physiology, including their regulation of gene expression. We began several years ago exploring the relationships between the NFkappaB transcription factor, neuronal survival, and glutamate receptor activation in telencephalic neurons. These studies led us to conclude that this population of cells is nearly incapable of activating the NFkappaB that is nonetheless expressed at reasonable levels. A subset of the kappaB cis elements are instead bound by members of the Sp1 family in neurons. Also surprising was our discovery that Sp1 itself, typically described as ubiquitous, is severely restricted in expression within forebrain neurons; Sp4 seems to be substituted during neuronal differentiation. These findings and their implications for neuronal differentiation--as well as potential dedifferentiation during degenerative processes--are discussed here.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsApolipoproteins EGlutamic AcidHumansI-kappa B ProteinsNeurogenesisNeurogenic InflammationNeuronsNF-kappa BProsencephalonSignal TransductionSp1 Transcription FactorSp4 Transcription FactorSuperoxide DismutaseApolipoproteins EGlutamic AcidI-kappa B ProteinsNF-kappa BSp1 Transcription FactorSp4 Transcription FactorSuperoxide DismutaseSuperoxide Dismutase 2Transcription Factor RelA

Identifiers

PMID19450264
PMCPMC2693111
OpenAlexW1975670052

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.