Evidence map›Paper›PMID 22294685›Full record

ArticleThe Journal of biological chemistry2012

Nurr1 protein is required for N-methyl-D-aspartic acid (NMDA) receptor-mediated neuronal survival.

Bruna Barneda-Zahonero, Joan-Marc Servitja, Nahuai Badiola, Alfredo J Miñano-Molina, Rut Fadó, Carlos A Saura, José Rodríguez-Alvarez

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. International journal of molecular sciences · 2024
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  9. Nurr1 Is Not an Essential Regulator of BDNF in Mouse Cortical Neurons.International journal of molecular sciences · 2022
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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

7 authors at 4 institutions in 1 country.

Bruna Barneda-ZahoneroInstitut de Neurociencies and Departament de Bioquímica i Biología Molecular, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Joan-Marc Servitja
Nahuai Badiola
Alfredo J Miñano-Molina
Rut Fadó
Carlos A Saura
José Rodríguez-Alvarez
Universitat Autònoma de Barcelona · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NMDA receptor (NMDAR) stimulation promotes neuronal survival during brain development. Cerebellar granule cells (CGCs) need NMDAR stimulation to survive and develop. These neurons differentiate and mature during its migration from the external granular layer to the internal granular layer, and lack of excitatory inputs triggers their apoptotic death. It is possible to mimic this process in vitro by culturing CGCs in low KCl concentrations (5 mm) in the presence or absence of NMDA. Using this experimental approach, we have obtained whole genome expression profiles after 3 and 8 h of NMDA addition to identify genes involved in NMDA-mediated survival of CGCs. One of the identified genes was Nurr1, a member of the orphan nuclear receptor subfamily Nr4a. Our results report a direct regulation of Nurr1 by CREB after NMDAR stimulation. ChIP assay confirmed CREB binding to Nurr1 promoter, whereas CREB shRNA blocked NMDA-mediated increase in Nurr1 expression. Moreover, we show that Nurr1 is important for NMDAR survival effect. We show that Nurr1 binds to Bdnf promoter IV and that silencing Nurr1 by shRNA leads to a decrease in brain-derived neurotrophic factor (BDNF) protein levels and a reduction of NMDA neuroprotective effect. Also, we report that Nurr1 and BDNF show a similar expression pattern during postnatal cerebellar development. Thus, we conclude that Nurr1 is a downstream target of CREB and that it is responsible for the NMDA-mediated increase in BDNF, which is necessary for the NMDA-mediated prosurvival effect on neurons.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCell SurvivalCyclic AMP Response Element-Binding ProteinGene SilencingNeuronsN-MethylaspartateNuclear Receptor Subfamily 4, Group A, Member 2RatsRats, WistarReceptors, N-Methyl-D-AspartateTranscriptional ActivationBrain-Derived Neurotrophic FactorCyclic AMP Response Element-Binding ProteinN-MethylaspartateNr4a2 protein, ratNuclear Receptor Subfamily 4, Group A, Member 2Receptors, N-Methyl-D-Aspartate

Identifiers

PMID22294685
PMCPMC3322860
OpenAlexW2053430540

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.