Literature DB >> 25988524

RSK3: A regulator of pathological cardiac remodeling.

Eliana C Martinez1, Catherine L Passariello1, Jinliang Li1, Christopher J Matheson2, Kimberly Dodge-Kafka3, Philip Reigan2, Michael S Kapiloff1.   

Abstract

The family of p90 ribosomal S6 kinases (RSKs) are pleiotropic effectors for extracellular signal-regulated kinase signaling pathways. Recently, RSK3 was shown to be important for pathological remodeling of the heart. Although cardiac myocyte hypertrophy can be compensatory for increased wall stress, in chronic heart diseases, this nonmitotic cell growth is usually associated with interstitial fibrosis, increased cell death, and decreased cardiac function. Although RSK3 is less abundant in the cardiac myocyte than other RSK family members, RSK3 appears to serve a unique role in cardiac myocyte stress responses. A potential mechanism conferring the unique function of RSK3 in the heart is anchoring by the scaffold protein muscle A-kinase anchoring protein β (mAKAPβ). Recent findings suggest that RSK3 should be considered as a therapeutic target for the prevention of heart failure, a clinical syndrome of major public health significance.
© 2015 International Union of Biochemistry and Molecular Biology.

Entities:  

Keywords:  Keywords ribosomal S6 kinase; heart; hypertrophy; mAKAP; remodeling; scaffold; signal transduction

Mesh:

Substances:

Year:  2015        PMID: 25988524      PMCID: PMC4449288          DOI: 10.1002/iub.1383

Source DB:  PubMed          Journal:  IUBMB Life        ISSN: 1521-6543            Impact factor:   3.885


  78 in total

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Authors:  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; Michael Sanders; Joshua M Hare; Andre Hanauer; Kimberly Dodge-Kafka; Michael S Kapiloff
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8.  The scaffold protein muscle A-kinase anchoring protein β orchestrates cardiac myocyte hypertrophic signaling required for the development of heart failure.

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10.  Targeted deletion of ERK2 in cardiomyocytes attenuates hypertrophic response but provokes pathological stress induced cardiac dysfunction.

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Journal:  J Mol Cell Cardiol       Date:  2014-03-12       Impact factor: 5.000

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Review 4.  Cardiac function modulation depends on the A-kinase anchoring protein complex.

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7.  RSK3 is required for concentric myocyte hypertrophy in an activated Raf1 model for Noonan syndrome.

Authors:  Catherine L Passariello; Eliana C Martinez; Hrishikesh Thakur; Maria Cesareo; Jinliang Li; Michael S Kapiloff
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  7 in total

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