Evidence map›Paper›PMID 23259949›Full record

ArticleNeuron2012

Activity-dependent transcriptional regulation of M-Type (Kv7) K(+) channels by AKAP79/150-mediated NFAT actions.

Jie Zhang, Mark S Shapiro

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

51 citing papers in PubMed, 82 citations in OpenAlex.

  1. Calcineurin inhibition may prevent Alzheimer disease in people with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  2. Article
  3. Article
  4. Cholinergic Stimulation Modulates the Functional Composition of CA3 Cell Types in the Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021
    Article
  12. CaCells · 2020
    Article
  13. Article
  14. Epileptic channelopathies caused by neuronal Kv7 (KCNQ) channel dysfunction.Pflugers Archiv : European journal of physiology · 2020
    Review
  15. Article
  16. Prevention of brain damage after traumatic brain injury by pharmacological enhancement of KCNQ (Kv7, "M-type") KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  17. Article
  18. The Role of KFrontiers in physiology · 2020
    Review
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Jie ZhangDepartment of Physiology, MS 7756, University of Texas Health Science Center, San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Mark S Shapiro
The University of Texas Health Science Center at San Antonio · US

Funding

Modulation of Neuronal Ion Channels by 2nd MessengersR01NS043394 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SHAPIRO, MARK S · 2002 to 2014
$4.5M
Mechanism and functional role of AKAP79/150 in M current control and excitabilityR01NS065138 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SHAPIRO, MARK S · 2009 to 2010
$788k
Mechanism and functional role of AKAP79/150 in M current controlR56NS065138 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SHAPIRO, MARK S · 2012 to 2012
$465k
NINDS NIH HHS ARRA R01 NS065138NINDS NIH HHS R01 NS043394NINDS NIH HHS R01 NS065138NINDS NIH HHS R01 NS43394NINDS NIH HHS R56 NS065138
6 · The paper itself

Abstract

M-type K(+) channels, encoded by KCNQ2-KCNQ5 genes, play key roles in regulation of neuronal excitability; however, less is known about the mechanisms controlling their transcriptional expression. Here, we discovered a mechanism regulating KCNQ2/3 transcriptional expression by neuronal activity in rodent neurons, involving activation of calcineurin and nuclear factor of activated T cell (NFAT) transcription factors, orchestrated by A kinase-anchoring protein (AKAP)79/150. The signal requires Ca(2+) influx through L-type Ca(2+) channels and both local and global Ca(2+) elevations. We postulate increased M-channel expression to act as a negative feedback to suppress neuronal hyperexcitability, demonstrated by profoundly upregulated KCNQ2/3 transcription in hippocampi from wild-type, but not AKAP150(-/-), mice after drug-induced seizures. Thus, we suggest a distinct role of AKAP79/150 and the complex it organizes in activity-dependent M-channel transcription, which may potentially serve throughout the nervous system to limit overexcitability associated with disease states such as epilepsy.

Indexed as

A Kinase Anchor ProteinsAnimalsCalcineurinGene Expression RegulationHippocampusKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelMiceMice, Inbred C57BLMice, KnockoutNeuronsNFATC Transcription FactorsSignal TransductionTranscriptional ActivationAkap5 protein, mouseA Kinase Anchor ProteinsCalcineurinKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelNFATC Transcription Factors

Identifiers

PMID23259949
PMCPMC3707625
OpenAlexW1976060371

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.