Undermining the endothelium by ablation of MAPK-MEF2 signaling
Eric N. Olson
Eric N. Olson
Published April 15, 2004
Citation Information: J Clin Invest. 2004;113(8):1110-1112. https://doi.org/10.1172/JCI21497.
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Commentary

Undermining the endothelium by ablation of MAPK-MEF2 signaling

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.

Authors

Eric N. Olson

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Figure 1

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MAPK signaling pathways. Survival signals activate MEKK2/3, which activa...
MAPK signaling pathways. Survival signals activate MEKK2/3, which activates MEK5, which activates BMK1. BMK1 stimulates the transcriptional activity of MEF2C by phosphorylating the transcription activation domain and by interacting directly with MEF2C and contributing its own transcriptional activation domain. MEF2C is required for cell survival and proliferation by activating downstream target genes that remain to be identified.