The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice
By O. Bueno, L. D. de Windt, Kevin M. Tymitz, S. Witt, T. Kimball, R. Klevitsky, T. Hewett, S. P. Jones, D. Lefer, C. Peng and 2 more. EMBO Journal, 2000
820 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0d7a223ea6407d7d0162cc2510832267967b0285
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In Cardiology and Cardiovascular Medicine
In Molecular Biology
Citations in the corpus
- Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. (2010, background): “In vivo, cardiac-specific expression of constitutively activated MEK1 also promotes hypertrophy (57).”
- Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “For instance, constitutive transgenic expression of MEK1 (upstream of ERK1/2) in mice induced an adaptive cardiac response (enhanced cardiac function with no fibrosis) (Bueno et al. 2000).”
- Germline gain-of-function mutations in SOS1 cause Noonan syndrome (2007, background): “A role for the Ras-Raf-MEK-ERK cascade in cardiac hypertrophy is supported by studies with transgenic mice in which cardiac-specific overexpression of activated MEK1 results in profound cardiac hypertrophy with preserved contractile functio”
- Cell and Molecular Biology (2009, background): “Specific activation of Erk in the heart leads to stable compensated (physiological) hypertrophy (Bueno et al., 2000).”
- Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “The importance of ERK MAPK signalling was proposed through the analysis of transgenic mice that express activated MEK1 under the transcriptional control of a cardiac-specific promoter, which showed specific activation of ERK1/2 in the hear”
- Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy (2007, background): “Transgenic mice expressing activated Hras or Mek1 develop cardiac hypertroph”