Evidence map›Paper›PMID 17316402›Full record

ArticleJournal of neurochemistry2007

Glutamate receptor activation evokes calpain-mediated degradation of Sp3 and Sp4, the prominent Sp-family transcription factors in neurons.

Xianrong Mao, Shao-Hua Yang, James W Simpkins, Steven W Barger

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. βIII-Tubulin Gene Regulation in Health and Disease.Frontiers in cell and developmental biology · 2022
    Review
  6. Purkinje Neurons with Loss of STIM1 Exhibit Age-Dependent Changes in Gene Expression and Synaptic Components.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  7. Review
  8. Maternal IL-17A in autism.Experimental neurology · 2018
    Review
  9. StableFrontiers in molecular neuroscience · 2018
    Article
  10. Mechanisms regulating dendritic arbor patterning.Cellular and molecular life sciences : CMLS · 2017
    Review
  11. Article
  12. Transcription factor SP4 phosphorylation is altered in the postmortem cerebellum of bipolar disorder and schizophrenia subjects.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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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 4 institutions in 1 country.

Xianrong MaoDepartment of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Shao-Hua Yang
James W Simpkins
Steven W Barger
Geriatric Research Education and Clinical Center · USUniversity of Arkansas for Medical Sciences · USUniversity of North Texas · USUniversity of North Texas Health Science Center · 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
NIA NIH HHS P01 AG012411NINDS NIH HHS R01 NS046439NINDS NIH HHS R01NS046439
6 · The paper itself

Abstract

Sp-family transcription factors (Sp1, Sp3 and Sp4) contain a zinc-finger domain that binds to DNA sequences rich in G-C/T. As assayed by RT-PCR analysis of mRNA, western-blot analysis, immunofluorescence, and antibody-dependent "supershift" of DNA-binding assays, the prominent Sp-family factors in cerebral neurons were identified as Sp3 and Sp4. By contrast, glial cells were found to express Sp1 and Sp3. We previously showed that the pattern of G-C/T binding activity of Sp-family factors is rapidly and specifically altered by the calcium influx accompanying activation of glutamate receptors. Here, we demonstrate that Sp-factor activity is also lost after a cerebral ischemia/reperfusion injury in vivo. Consistent with its calcium-dependent nature, we found that glutamate's effect on Sp-family factors could be blocked by inhibitors of calpains, neutral cysteine proteases activated by calcium. Purified calpain I cleaved Sp3 and Sp4 into products that retained G-C/T-binding activity, consistent with species observed in glutamate-treated neurons. These data provide details of an impact of glutamate-receptor activation on molecular events connected to gene expression.

Indexed as

AnimalsCalpainCells, CulturedCerebral CortexExcitatory Amino Acid AgonistsGlutamic AcidIschemic Attack, TransientNeuronsRatsRats, Sprague-DawleyReceptors, GlutamateReperfusion InjurySp1 Transcription FactorSp3 Transcription FactorSp4 Transcription FactorCalpainExcitatory Amino Acid AgonistsGlutamic AcidReceptors, GlutamateSp1 Transcription FactorSp3 protein, ratSp3 Transcription FactorSp4 protein, ratSp4 Transcription Factor

Identifiers

PMID17316402
PMCPMC1949346
OpenAlexW1812789581

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.