Evidence map›Paper›PMID 20519532›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

The DREAM protein negatively regulates the NMDA receptor through interaction with the NR1 subunit.

Ying Zhang, Ping Su, Ping Liang, Tao Liu, Xu Liu, Xin-Ying Liu, Bo Zhang, Tao Han, Yan-Bing Zhu, Dong-Min Yin and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. KCells · 2023
    Review
  4. Emerging Role of DREAM in Healthy Brain and Neurological Diseases.International journal of molecular sciences · 2023
    Review
  5. Article
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  10. Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Review
  11. Global Gene Knockout ofFrontiers in molecular neuroscience · 2019
    Article
  12. Article
  13. KChIP3 N-Terminal 31-50 Fragment Mediates Its Association with TRPV1 and Alleviates Inflammatory Hyperalgesia in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    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

14 authors at 3 institutions in 2 countries.

Ying ZhangNeuroscience Research Institute, Key Laboratory for Neuroscience of Ministry of Education and Health, Peking University, Beijing, China.
Ping Su
Ping Liang
Tao Liu
Xu Liu
Xin-Ying Liu
Bo Zhang
Tao Han
Yan-Bing Zhu
Dong-Min Yin
Junfa Li
Zhuan Zhou
Ke-Wei Wang
Yun Wang
Peking University · CNCapital Medical University · CNCapital University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutamate-induced excitotoxicity has been implicated in the etiology of stroke, epilepsy, and neurodegenerative diseases. NMDA receptors (NMDARs) play a pivotal role in excitotoxic injury; however, clinical trials testing NMDAR antagonists as neuroprotectants have been discouraging. The development of novel neuroprotectant molecules is being vigorously pursued. Here, we report that downstream regulatory element antagonist modulator (DREAM) significantly inhibits surface expression of NMDARs and NMDAR-mediated current. Overexpression of DREAM showed neuroprotection against excitotoxic neuronal injury, whereas knockdown of DREAM enhanced NMDA-induced toxicity. DREAM could directly bind to the C0 domain of the NR1 subunit. Although DREAM contains multiple binding sites for the NR1 subunit, residues 21-40 of the N terminus are the main binding site for the NR1 subunit. Thus, 21-40 residues might relieve the autoinhibition conferred by residues 1-50 and derepress the DREAM core domain by a competitive mechanism. Intriguingly, the cell-permeable TAT-21-40 peptide, constructed according to the critical binding site of DREAM to the NR1 subunit, inhibits NMDAR-mediated currents in primary cultured hippocampal neurons and has a neuroprotective effect on in vitro neuronal excitotoxic injury and in vivo ischemic brain damage. Moreover, both pretreatment and posttreatment of TAT-21-40 is effective against excitotoxicity. In summary, this work reveals a novel, negative regulator of NMDARs and provides an attractive candidate for the treatment of excitotoxicity-related disease.

Indexed as

Analysis of VarianceAnimalsBiotinylationBrain EdemaBrain InfarctionBrain IschemiaCell CountCells, CulturedCHO CellsCricetinaeCricetulusDisease Models, AnimalDose-Response Relationship, DrugEmbryo, MammalianExcitatory Amino Acid AgonistsGene Expression RegulationExcitatory Amino Acid AgonistsGlucoseGreen Fluorescent ProteinsKCNIP3 protein, humanKv Channel-Interacting ProteinsL-Lactate DehydrogenaseNeuroprotective AgentsN-MethylaspartateNR1 NMDA receptorPeptidesReceptors, N-Methyl-D-AspartateRepressor ProteinsRNA, Small Interfering

Identifiers

PMID20519532
PMCPMC6632380
OpenAlexW2134629226

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.