Evidence map›Paper›PMID 17287525›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Hypo-osmolar stress induces p75NTR expression by activating Sp1-dependent transcription.

Alberto Ramos, Wai Chi Ho, Stephanie Forte, Kathleen Dickson, Jacqueline Boutilier, Kristy Favell, Philip A Barker

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Implication of the neurotrophin receptor p75Expert review of ophthalmology · 2017
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Mir-592 regulates the induction and cell death-promoting activity of p75NTR in neuronal ischemic injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  16. Article
  17. Article
  18. Review
  19. p75 neurotrophin receptor is a clock gene that regulates oscillatory components of circadian and metabolic networks.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    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

7 authors at 4 institutions in 3 countries.

Alberto RamosMontreal Neurological Institute, McGill University, Montreal, Quebec, Canada H3A 2B4.
Wai Chi Ho
Stephanie Forte
Kathleen Dickson
Jacqueline Boutilier
Kristy Favell
Philip A Barker
Cornell University · USMcGill University · CAMontreal Neurological Institute and Hospital · CASaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Injury-induced expression of the p75 neurotrophin receptor (p75NTR) in the CNS facilitates neuronal apoptosis and prevents neuronal regrowth, but the mechanisms regulating p75NTR expression are poorly characterized. In this study, we showed that hypo-osmolarity induces p75NTR expression in primary neurons, and, using a comparative genomics approach, we identified conserved elements in the 25 kb upstream sequences of the rat, mouse, and human p75NTR genes. We found that only one of these, a proximal region rich in Sp1 sites, responds to changes in hypo-osmolarity. We then showed that Sp1 DNA binding activity is increased in cells exposed to hypo-osmolarity, established that hypo-osmolarity enhanced Sp1 binding to the endogenous p75NTR promoter, and showed that Sp1 is required for p75NTR expression induced by hypo-osmolarity. We examined how Sp1 is regulated to effect these changes and established that Sp1 turnover is strongly inhibited by hypo-osmolarity. We propose that stress-induced Sp1 accumulation that results from reductions in Sp1 turnover rate contributes to injury-induced gene expression.

Indexed as

AnimalsBinding SitesCell LineCerebral CortexConsensus SequenceCycloheximideDNAElectrophoretic Mobility Shift AssayGene Expression RegulationGenes, DominantHumansHypotonic SolutionsKidneyMiceMutationNerve Tissue ProteinsCycloheximideDNAHypotonic SolutionsNerve Tissue ProteinsNGFR protein, humanNgfr protein, mouseNgfr protein, ratPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase CReceptors, Growth FactorReceptors, Nerve Growth FactorRecombinant Fusion ProteinsRNA, MessengerRNA, Small InterferingSp1 Transcription FactorSP3 protein, humanSp3 Transcription FactorType C Phospholipases

Identifiers

PMID17287525
PMCPMC6673569
OpenAlexW2141720838

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.