Evidence map›Paper›PMID 21738458›Full record

ArticlePLoS computational biology2011

Colocalization of protein kinase A with adenylyl cyclase enhances protein kinase A activity during induction of long-lasting long-term-potentiation.

Myungsook Kim, Alan Jung Park, Robbert Havekes, Andrew Chay, Leonardo Antonio Guercio, Rodrigo Freire Oliveira, Ted Abel, Kim T Blackwell

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 54 citations in OpenAlex.

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  12. Competitive Tuning Among CaCellular and molecular bioengineering · 2018
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  18. Genealogical correspondence of a forebrain centre implies an executive brain in the protostome-deuterostome bilaterian ancestor.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    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

8 authors at 2 institutions in 1 country.

Myungsook KimGeorge Mason University, The Krasnow Institute for Advanced Studies, Fairfax, Virginia, United States of America.
Alan Jung Park
Robbert Havekes
Andrew Chay
Leonardo Antonio Guercio
Rodrigo Freire Oliveira
Ted Abel
Kim T Blackwell
George Mason University · USUniversity of Pennsylvania · US

Funding

SYSTEMS AND INTEGRATIVE BIOLOGYT32GM007517 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI GOLD, JOSHUA I · 1985 to 2017
$8.0M
CRCNS: Spatial & Temporal Aspects of cAMP/PKA Signaling Underlying InformationR01AA018060 · NIAAA · GEORGE MASON UNIVERSITY · PI ABEL, EDWIN TED G., BLACKWELL, KIM L · 2008 to 2012
$1.8M
NIAAA NIH HHS R01 AA018060NIAAA NIH HHS R01 AA18060NIGMS NIH HHS T32 GM007517
6 · The paper itself

Abstract

The ability of neurons to differentially respond to specific temporal and spatial input patterns underlies information storage in neural circuits. One means of achieving spatial specificity is to restrict signaling molecules to particular subcellular compartments using anchoring molecules such as A-Kinase Anchoring Proteins (AKAPs). Disruption of protein kinase A (PKA) anchoring to AKAPs impairs a PKA-dependent form of long term potentiation (LTP) in the hippocampus. To investigate the role of localized PKA signaling in LTP, we developed a stochastic reaction-diffusion model of the signaling pathways leading to PKA activation in CA1 pyramidal neurons. Simulations investigated whether the role of anchoring is to locate kinases near molecules that activate them, or near their target molecules. The results show that anchoring PKA with adenylyl cyclase (which produces cAMP that activates PKA) produces significantly greater PKA activity, and phosphorylation of both inhibitor-1 and AMPA receptor GluR1 subunit on S845, than when PKA is anchored apart from adenylyl cyclase. The spatial microdomain of cAMP was smaller than that of PKA suggesting that anchoring PKA near its source of cAMP is critical because inactivation by phosphodiesterase limits diffusion of cAMP. The prediction that the role of anchoring is to colocalize PKA near adenylyl cyclase was confirmed by experimentally rescuing the deficit in LTP produced by disruption of PKA anchoring using phosphodiesterase inhibitors. Additional experiments confirm the model prediction that disruption of anchoring impairs S845 phosphorylation produced by forskolin-induced synaptic potentiation. Collectively, these results show that locating PKA near adenylyl cyclase is a critical function of anchoring.

Indexed as

Adenylyl CyclasesA Kinase Anchor ProteinsAnimalsCA1 Region, HippocampalCalciumColforsinComputer SimulationCyclic AMPCyclic AMP-Dependent Protein KinasesDiffusionDopamineLong-Term PotentiationMiceModels, BiologicalProteinsPyramidal CellsAdenylyl CyclasesA Kinase Anchor ProteinsCalciumColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesDopamineHt 31 protein, syntheticProteins

Identifiers

PMID21738458
PMCPMC3127802
OpenAlexW1975246673

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.