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Article

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

Journal of molecular and cellular cardiology - 1 Apr 2016

Passariello Catherine L, Martinez Eliana C, Thakur Hrishikesh, Cesareo Maria, Li Jinliang, Kapiloff Michael S

Abstract excerpt

Noonan syndrome (NS) is a congenital disorder resulting from mutations of the Ras-Raf signaling pathway. Hypertrophic cardiomyopathy associated with RAF1 "RASopathy" mutations is a major risk factor for heart failure and death in NS and has been attributed to activation of MEK1/2-ERK1/2 mitogen-activated protein kinases. We recently discovered that type 3 p90 ribosomal S6 kinase (RSK3) is an ERK effector that is...

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Share to Cardiomyopathy, Hypertrophic
Share to Echocardiography

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Enzyme Activation

Share to MAP Kinase Signaling System

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Share to Proto-Oncogene Proteins c-raf

Share to Ribosomal Protein S6 Kinases, 90-kDa

Share to Ventricular Remodeling

Source

Open in PubMed Open full text

Identifiers

PMID: 26940993
DOI: 10.1016/j.yjmcc.2016.02.020
PMCID: PMC4846495

Genes

RAF1

Provenance

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Related research

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Research trail→

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RSK3 is required for concentric myocyte hypertrophy in an activated Raf1 model for Noonan syndrome.PMID 26940993Read ↗

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