Evidence map›Paper›PMID 29704264›Full record

ArticleGlia2018

NF-Y-dependent regulation of glutamate receptor 4 expression and cell survival in cells of the oligodendrocyte lineage.

Ghazala Begum, Masahiro Otsu, Usman Ahmed, Zubair Ahmed, Adam Stevens, Daniel Fulton

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. CaThe Journal of physiology · 2021
    Article
  7. Glial Cell AMPA Receptors in Nervous System Health, Injury and Disease.International journal of molecular sciences · 2019
    Review
  8. Article
  9. Review
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

6 authors at 2 institutions in 1 country.

Ghazala BegumNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.
Masahiro OtsuNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.
Usman AhmedNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.
Zubair AhmedNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.ORCID 0000-0001-6267-6442
Adam StevensDivision of Developmental Biology & Medicine, Faculty of Biology, Medicine & Health, University of Manchester, Manchester Academic Health Sciences Centre, Manchester M13 9PL, United Kingdom.ORCID 0000-0002-1950-7325
Daniel FultonNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.ORCID 0000-0002-5712-2776
University of Birmingham · GBManchester Academic Health Science Centre · GB

Funding

European Commission Horizon 2020 Framework Program (Marie Sklowdoswka-Curie Actions Individual Fellowship) 659279University of BirminghamWellcome TrustWellcome Trust Institutional Strategic Support Fund
6 · The paper itself

Abstract

Glutamate receptor subunit 4 (GluA4) is highly expressed by neural cells sensitive to excitotoxicity, and is the predominant subunit expressed by oligodendrocyte precursor cells (OPC) during a key period of vulnerability to hypoxic-ischemic injury. Therefore, transcriptional networks downstream of excitotoxic GluA4 activation represent a promising area for therapeutic intervention. In this work, we identify the CCAAT binding transcription factor NF-Yb as a novel transcriptional regulator of Gria4 (GluA4 gene), and a controller of excitotoxic death in the oligodendroglial lineage. We describe a novel regulatory region within Gria4 containing CCAAT sequences whose binding by NF-Yb is regulated by excitotoxicity. Excitotoxicity-induced alterations in NF-Yb binding are associated with changes in Gria4 transcription, while knockdown of NF-Yb alters the transcription of reporter constructs containing this regulatory region. Data from immortalized and primary OPC reveal that RNAi and pharmacological disruption of NF-Yb alter Gria4 transcription, with the latter inducing apoptosis and influencing a set of apoptotic genes similarly regulated during excitotoxicity. These data provide the first definition of a trans-acting mechanism regulating Gria4, and identify the NF-Y network as a potential source of pharmacological targets for promoting OPC survival.

Indexed as

AnimalsApoptosisCCAAT-Binding FactorCell LineCells, CulturedCell SurvivalE1A-Associated p300 ProteinGene Expression RegulationMice, Inbred C57BLNeocortexOligodendrocyte Precursor CellsOligodendrogliaReceptors, AMPARegulatory Sequences, Nucleic AcidTerpenesTranscription, GeneticCCAAT-Binding FactorE1A-Associated p300 ProteinEp300 protein, mousegarcinolglutamate receptor ionotropic, AMPA 4Nfyb protein, mouseReceptors, AMPATerpenesAMPA receptorCCAATexcitotoxicityGluA4Gria4NF-Yboligodendrocyte precursor cellOli-neutranscriptional regulation

Identifiers

PMID29704264
PMCPMC6220837
OpenAlexW2800538317

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.