Evidence map›Paper›PMID 19955386›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Nuclear factor of activated T-cells isoform c4 (NFATc4/NFAT3) as a mediator of antiapoptotic transcription in NMDA receptor-stimulated cortical neurons.

Aruna Vashishta, Agata Habas, Priit Pruunsild, Jing-Juan Zheng, Tõnis Timmusk, Michal Hetman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
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

47 citing papers in PubMed, 69 citations in OpenAlex.

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  12. CREB Family Transcription Factors Are Major Mediators of BDNF Transcriptional Autoregulation in Cortical Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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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

6 authors at 3 institutions in 2 countries.

Aruna VashishtaKentucky Spinal Cord Injury Research Center and Department of Neurological Surgery, University of Louisville, Louisville, Kentucky 40292, USA.
Agata Habas
Priit Pruunsild
Jing-Juan Zheng
Tõnis Timmusk
Michal Hetman
Neurological Surgery · USTallinn University of Technology · EEUniversity of Louisville · US

Funding

Signaling pathways in neuronal susceptibility to hypoxiaP20RR015576 · NCRR · UNIVERSITY OF LOUISVILLE · PI HUBSCHER, CHARLES H. · 2000 to 2009
$18.5M
Survival signaling in CNS neurons exposed to DNA damageR01NS047341 · NINDS · UNIVERSITY OF LOUISVILLE · PI HETMAN, MICHAL · 2004 to 2008
$1.3M
Synuclein Binding Proteins: Conformational RegulatorsR21NS043741 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LAURING, BRETT P · 2003 to 2003
$194k
NCRR NIH HHS P20 RR015576NCRR NIH HHS RR015576-06NINDS NIH HHS NS043741-01NINDS NIH HHS R01 NS047341
6 · The paper itself

Abstract

During cortical development, when NR2B subunit is the major component of the NMDA glutamate receptors (NMDARs), moderate NMDAR activity supports neuronal survival at least in part by regulating gene transcription. We report that, in cultured cortical neurons from newborn rats, the NMDARs activated the calcium-responsive transcription regulator nuclear factor of activated T cells (NFAT). Moreover, in developing rat cortex, the NFAT isoforms c3 and c4 (NFATc3 and NFATc4) were expressed at relatively higher levels at postnatal day 7 (P7) than P21, overlapping with the period of NMDAR-dependent survival. In cultured cortical neurons, NFATc3 and NFATc4 were regulated at least in part by the NR2B NMDAR. Conversely, knockdown of NFATc4 but not NFATc3 induced cortical neuron apoptosis. Likewise, NFATc4 inhibition prevented antiapoptotic neuroprotection in response to exogenous NMDA. Expression of the brain-derived neurotrophic factor (BDNF) was reduced by NFATc4 inhibition. NFATc4 regulated transcription by the NMDAR-responsive bdnf promoter IV. In addition, NMDAR blockers including NR2B-selective once reduced BDNF expression in P7 cortex and cultured cortical neurons. Finally, exogenous BDNF rescued from the proapoptotic effects of NFATc4 inhibition. These results identify bdnf as one of the target genes for the antiapoptotic signaling by NMDAR-NFATc4. Thus, the previously unrecognized NMDAR-NFATc4-BDNF pathway contributes to the survival signaling network that supports cortical development.

Indexed as

Age FactorsAnimalsAnimals, NewbornApoptosisBrain-Derived Neurotrophic FactorCells, CulturedCerebral CortexEnzyme InhibitorsExcitatory Amino Acid AntagonistsGABA AgentsGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsMaleNeuronsNFATC Transcription FactorsRatsBrain-Derived Neurotrophic FactorEnzyme InhibitorsExcitatory Amino Acid AntagonistsGABA AgentsGreen Fluorescent ProteinsNFATC Transcription FactorsNR2A NMDA receptorReceptors, N-Methyl-D-AspartateRNA, MessengerRNA, Small InterferingSodium Channel BlockersTetrodotoxin

Identifiers

PMID19955386
PMCPMC2836809
OpenAlexW2162441710

What OpenQuestion holds

Textmetadata
LicenceTDM
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.