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Updated: Jul 11, 2026

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Published on: June 11, 2017
Undermining the endothelium by ablation of MAPK-MEF2 signaling
1Department of Molecular Biology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9148, USA. eric.olsen@UTSouthwestern.edu
Abstract:
Numerous stimuli activate Big MAPK-1 (BMK1), an MAPK that activates the myocyte enhancer factor-2 (MEF2) transcription factor. Conditional gene deletion showed BMK1 to be required for survival of endothelial cells. An active form of MEF2C could partially bypass the requirement for BMK1 for endothelial cell survival in vitro. These findings reveal an essential role for BMK1-MEF2 signaling in an endothelial cell survival pathway and raise interesting questions about the molecular basis of this response.
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