Evidence map›Paper›PMID 22174809›Full record

ArticlePloS one2011

Regulation of brain-derived neurotrophic factor exon IV transcription through calcium responsive elements in cortical neurons.

Fei Zheng, Xianju Zhou, Yongneng Luo, Hua Xiao, Gary Wayman, Hongbing Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

46 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
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  3. Review
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  6. Review
  7. Article
  8. CaFrontiers in pharmacology · 2022
    Review
  9. Genetic removal of synaptic ZnFrontiers in neurology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. 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

6 authors at 3 institutions in 1 country.

Fei ZhengDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan, United States of America.
Xianju Zhou
Yongneng Luo
Hua Xiao
Gary Wayman
Hongbing Wang
Michigan State University · USMichigan United · USWashington State University · US

Funding

Control of Dendritic and Synaptic Development by Extracellular CuesR01MH086032 · NIMH · WASHINGTON STATE UNIVERSITY · PI WAYMAN, GARY ALLEN · 2010 to 2014
$1.8M
The Role of A Transcription Cofactor in TumorigenesisR01DK066110 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIAO, HUA · 2004 to 2008
$1.3M
Regulation of BDNF Expression by Calcium-stimulated Protein KinasesR01MH076906 · NIMH · MICHIGAN STATE UNIVERSITY · PI WANG, HONGBING · 2007 to 2010
$1.2M
NIDDK NIH HHS DK066110NIDDK NIH HHS R01 DK066110NIMH NIH HHS MH076906NIMH NIH HHS MH086032NIMH NIH HHS R01 MH076906NIMH NIH HHS R01 MH086032
6 · The paper itself

Abstract

Activity-dependent transcription of brain-derived neurotrophic factor (BDNF) has been studied as an important model to elucidate the mechanisms underlying numerous aspects of neuroplasticity. It has been extensively emphasized that Ca(2+) influx through different routes may have significantly different effects on BDNF transcription. Here, we examined the regulatory property of the major calcium responsive elements (CaRE) in BDNF promoter IV in cultured rat cortical neurons. BDNF promoter IV, as well as CaRE1 and CaRE3, was significantly activated by Ca(2+) influx through L-type voltage-gated calcium channel (L-VGCC) or NMDA receptor (NMDAR). However, the L-VGCC- and NMDAR-mediated activation of CaRE was differentially regulated by different Ca(2+)-stimulated protein kinases. Specifically, PKA, CaMKI, and CaMKIV activity were required for L-VGCC-, but not NMDAR-mediated CaRE1 activation. CaMKI activity was required for NMDAR- but not L-VGCC-mediated CaRE3 activation. Surprisingly, the activation of CaRF, a previously identified transcription factor for CaRE1, was stimulated via L-VGCC but not NMDAR, and required MEK, PI3K and CaMKII activity. These results suggest a new working model that activity-dependent BDNF IV up-regulation may be coordinately mediated by CaRE1 and CaRE3 activity, which show different responses to Ca(2+)-stimulated kinases. Our data also explain how the individual cis-element in BDNF promoter is distinctively coupled to different Ca(2+) routes.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCalciumCalcium ChannelsCerebral CortexCyclic AMP Response Element-Binding ProteinExonsGene Expression RegulationLuciferasesModels, BiologicalNeuronsN-MethylaspartatePotassium ChlorideProtein KinasesRatsRats, Sprague-DawleyBrain-Derived Neurotrophic FactorCalciumCalcium ChannelsCyclic AMP Response Element-Binding ProteinLuciferasesN-MethylaspartatePotassium ChlorideProtein KinasesReceptors, N-Methyl-D-AspartateRNA, Messenger

Identifiers

PMID22174809
PMCPMC3235121
OpenAlexW2015703332

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.