Evidence map›Paper›PMID 21273417›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

AKAP79/150 impacts intrinsic excitability of hippocampal neurons through phospho-regulation of A-type K+ channel trafficking.

Lin Lin, Wei Sun, Faith Kung, Mark L Dell'Acqua, Dax A Hoffman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

35 citing papers in PubMed, 54 citations in OpenAlex.

  1. Calcineurin in cancer signaling networks.Nagoya journal of medical science · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. R-type voltage-gated CaCell reports · 2022
    Article
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  20. Calcineurin signaling in the heart: The importance of time and place.Journal of molecular and cellular cardiology · 2017
    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

5 authors at 3 institutions in 2 countries.

Lin LinEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Wei Sun
Faith Kung
Mark L Dell'Acqua
Dax A Hoffman
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USPeking University · CNUniversity of Colorado Denver · US

Funding

Potassium Channels and Dendritic Function in Hippocampal Pyramidal NeuronsZIAHD008755 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI HOFFMAN, DAX A · 2009 to 2025
$29.6M
Regulation of Calcium-permeable AMPA Receptors by AKAP79 Postsynaptic SignalingR01NS040701 · NINDS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 2001 to 2023
$7.7M
AKAP Regulation of Neuronal L-type Calcium Channel Signaling to the NucleusR01MH080291 · NIMH · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 2008 to 2013
$2.2M
Intramural NIH HHS Z99 HD999999Intramural NIH HHS ZIA HD008755NIMH NIH HHS R01 MH080291NINDS NIH HHS R01 NS040701
6 · The paper itself

Abstract

Kv4.2, as the primary α-subunit of rapidly inactivating, A-type voltage-gated K(+) (Kv) channels expressed in hippocampal CA1 pyramidal dendrites, plays a critical role in regulating their excitability. Activity-dependent trafficking of Kv4.2 relies on C-terminal protein kinase A (PKA) phosphorylation. A-kinase-anchoring proteins (AKAPs) target PKA to glutamate receptor and ion channel complexes to allow for discrete, local signaling. As part of a previous study, we showed that AKAP79/150 interacts with Kv4.2 complexes and that the two proteins colocalize in hippocampal neurons. However, the nature and functional consequence of their interaction has not been previously explored. Here, we report that the C-terminal domain of Kv4.2 interacts with an internal region of AKAP79/150 that overlaps with its MAGUK (membrane-associated guanylate kinase)-binding domain. We show that AKAP79/150-anchored PKA activity controls Kv4.2 surface expression in heterologous cells and hippocampal neurons. Consistent with these findings, disrupting PKA anchoring led to a decrease in neuronal excitability, while preventing dephosphorylation by the phosphatase calcineurin resulted in increased excitability. These results demonstrate that AKAP79/150 provides a platform for dynamic PKA regulation of Kv4.2 expression, fundamentally impacting CA1 excitability.

Indexed as

Action PotentialsA Kinase Anchor ProteinsAnimalsBinding SitesCells, CulturedCyclic AMP-Dependent Protein KinasesGuanylate KinasesHippocampusMutationNeuronsPDZ DomainsPhosphorylationProtein BindingProtein TransportRatsShal Potassium ChannelsAkap5 protein, ratA Kinase Anchor ProteinsCyclic AMP-Dependent Protein KinasesGuanylate KinasesShal Potassium Channels

Identifiers

PMID21273417
PMCPMC3035425
OpenAlexW2108247031

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.