Evidence map›Paper›PMID 25547489›Full record

ReviewInternational journal of molecular sciences2014

Compartmentalization role of A-kinase anchoring proteins (AKAPs) in mediating protein kinase A (PKA) signaling and cardiomyocyte hypertrophy.

Abeer Rababa'h, Sonal Singh, Santosh V Suryavanshi, Salah Eldien Altarabsheh, Salil V Deo, Bradley K McConnell

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2014. 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
2.6field-weighted citation impact, top 10% 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, 41 citations in OpenAlex.

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  14. Form follows function: polymorphisms in mAKAP alter cardiac cAMP/PKA signaling.American journal of physiology. Heart and circulatory physiology · 2018
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  19. Loss ofFrontiers in physiology · 2018
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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 4 institutions in 2 countries.

Abeer Rababa'hDepartment of Clinical Pharmacy, Jordan University of Science and Technology, Irbid 22110, Jordan. amrababah@just.edu.jo.
Sonal SinghDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Texas Medical Center, Houston, TX 77204, USA. svsuryavanshi@uh.edu.
Santosh V SuryavanshiDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Texas Medical Center, Houston, TX 77204, USA. svsuryavanshi@uh.edu.
Salah Eldien AltarabshehDepartment of Cardiac Surgery, Queen Alia Heart Institute, Amman 11953, Jordan. Salah936@yahoo.com.
Salil V DeoDepartment of Cardiovascular Surgery, Case Western Reserve University, Cleveland, OH 44106, USA. Salildeo@yahoo.co.in.
Bradley K McConnellDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Texas Medical Center, Houston, TX 77204, USA. bkmcconn@central.uh.edu.
Texas Medical Center · USCase Western Reserve University · USJordan Hospital · JOJordan University of Science and Technology · JO

Funding

Targeted Disruption of Beta-Adrenergic Signaling to Increase Cardiac ContractilitR01HL085487 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI MCCONNELL, BRADLEY K · 2007 to 2011
$2.3M
Scaffolding Protein Interaction Network Regulates Cardiac Cell SignalingR15HL124458 · NHLBI · UNIVERSITY OF HOUSTON · PI MCCONNELL, BRADLEY K · 2015 to 2015
$452k
NHLBI NIH HHS HL085487NHLBI NIH HHS R01 HL085487NHLBI NIH HHS R15 HL124458
6 · The paper itself

Abstract

The Beta-adrenergic receptors (β-ARs) stimulation enhances contractility through protein kinase-A (PKA) substrate phosphorylation. This PKA signaling is conferred in part by PKA binding to A-kinase anchoring proteins (AKAPs). AKAPs coordinate multi-protein signaling networks that are targeted to specific intracellular locations, resulting in the localization of enzyme activity and transmitting intracellular actions of neurotransmitters and hormones to its target substrates. In particular, mAKAP (muscle-selective AKAP) has been shown to be present on the nuclear envelope of cardiomyocytes with various proteins including: PKA-regulatory subunit (RIIα), phosphodiesterase-4D3, protein phosphatase-2A, and ryanodine receptor (RyR2). Therefore, through the coordination of spatial-temporal signaling of proteins and enzymes, mAKAP controls cyclic-adenosine monophosphate (cAMP) levels very tightly and functions as a regulator of PKA-mediated substrate phosphorylation leading to changes in calcium availability and myofilament calcium sensitivity. The goal of this review is to elucidate the critical compartmentalization role of mAKAP in mediating PKA signaling and regulating cardiomyocyte hypertrophy by acting as a scaffolding protein. Based on our literature search and studying the structure-function relationship between AKAP scaffolding protein and its binding partners, we propose possible explanations for the mechanism by which mAKAP promotes cardiac hypertrophy.

Indexed as

Signal TransductionA Kinase Anchor ProteinsAnimalsCardiomegalyCyclic AMP-Dependent Protein KinasesHumansMyocytes, CardiacProtein TransportA Kinase Anchor ProteinsCyclic AMP-Dependent Protein Kinases

Identifiers

PMID25547489
PMCPMC4307244
OpenAlexW2052656852

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.