Evidence map›Paper›PMID 22997248›Full record

ArticleCirculation research2013

Anchored p90 ribosomal S6 kinase 3 is required for cardiac myocyte hypertrophy.

Jinliang Li, Michael D Kritzer, Jennifer J Carlisle Michel, Andrew Le, Hrishikesh Thakur, Marjorie Gayanilo, Catherine L Passariello, Alejandra Negro, Joshua B Danial, Behzad Oskouei and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

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  17. The NCirculation · 2019
    Article
  18. Bidirectional regulation of HDAC5 by mAKAPβ signalosomes in cardiac myocytes.Journal of molecular and cellular cardiology · 2018
    Article
  19. Review
  20. Function of Adenylyl Cyclase in Heart: the AKAP Connection.Journal of cardiovascular development and disease · 2018
    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

15 authors at 1 institution in 3 countries.

Jinliang LiCardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, Department of Pediatrics, University of Miami Leonard M. Miller School of Medicine, R198, P.O. Box 016960, Miami, FL 33101, USA.
Michael D Kritzer
Jennifer J Carlisle Michel
Andrew Le
Hrishikesh Thakur
Marjorie Gayanilo
Catherine L Passariello
Alejandra Negro
Joshua B Danial
Behzad Oskouei
Michael Sanders
Joshua M Hare
Andre Hanauer
Kimberly Dodge-Kafka
Michael S Kapiloff
Centre National de la Recherche Scientifique · FR

Funding

Role of the mAKAP Complex in Cardiac HypertrophyR01HL075398 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI KAPILOFF, MICHAEL SETH · 2004 to 2014
$3.6M
mAKAP-orchestrated phosphorylation events: regulation of PDE4D3R01HL082705 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DODGE-KAFKA, KIMBERLY L · 2006 to 2010
$1.8M
NHLBI NIH HHS HL075398NHLBI NIH HHS HL82705NHLBI NIH HHS R01 HL075398NHLBI NIH HHS R01 HL082705
6 · The paper itself

Abstract

rationaleCardiac myocyte hypertrophy is the main compensatory response to chronic stress on the heart. p90 ribosomal S6 kinase (RSK) family members are effectors for extracellular signal-regulated kinases that induce myocyte growth. Although increased RSK activity has been observed in stressed myocytes, the functions of individual RSK family members have remained poorly defined, despite being potential therapeutic targets for cardiac disease.

objectiveTo demonstrate that type 3 RSK (RSK3) is required for cardiac myocyte hypertrophy. METHODS AND

resultsRSK3 contains a unique N-terminal domain that is not conserved in other RSK family members. We show that this domain mediates the regulated binding of RSK3 to the muscle A-kinase anchoring protein scaffold, defining a novel kinase anchoring event. Disruption of both RSK3 expression using RNA interference and RSK3 anchoring using a competing muscle A-kinase anchoring protein peptide inhibited the hypertrophy of cultured myocytes. In vivo, RSK3 gene deletion in the mouse attenuated the concentric myocyte hypertrophy induced by pressure overload and catecholamine infusion.

conclusionsTaken together, these data demonstrate that anchored RSK3 transduces signals that modulate pathologic myocyte growth. Targeting of signaling complexes that contain select kinase isoforms should provide an approach for the specific inhibition of cardiac myocyte hypertrophy and for the development of novel strategies for the prevention and treatment of heart failure.

Indexed as

Adaptor Proteins, Signal TransducingA Kinase Anchor ProteinsAnimalsAnimals, NewbornBinding SitesCardiomegalyChlorocebus aethiopsCOS CellsDisease Models, AnimalFemaleGenotypeHEK293 CellsHumansImmunoprecipitationIsoproterenolMaleAdaptor Proteins, Signal TransducingAkap6 protein, ratA Kinase Anchor ProteinsIsoproterenolmAkap6 protein, mouseribosomal protein S6 kinase, 90kDa, polypeptide 3Ribosomal Protein S6 Kinases, 90-kDa

Identifiers

PMID22997248
PMCPMC3537852
OpenAlexW2158326728

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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.