Undermining the endothelium by ablation of MAPK-MEF2 signaling.
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.
Olson
Eric N
EN
Department of Molecular Biology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9148, USA. eric.olsen@UTSouthwestern.edu
D000818:Animals; D002470:Cell Survival; D004268:DNA-Binding Proteins / Q000502:physiology*; D042783:Endothelial Cells / Q000502:physiology*; D007333:Insulin Resistance; D020935:MAP Kinase Signaling System / Q000502:physiology*; D064326:MEF2 Transcription Factors; D051379:Mice; D018345:Mice, Knockout; D048054:Mitogen-Activated Protein Kinase 7; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000502:physiology*; D018006:Myogenic Regulatory Factors; D014157:Transcription Factors / Q000502:physiology*
D004268:DNA-Binding Proteins; D064326:MEF2 Transcription Factors; C578041:Mef2c protein, mouse; D018006:Myogenic Regulatory Factors; D014157:Transcription Factors; D048054:Mitogen-Activated Protein Kinase 7; D020928:Mitogen-Activated Protein Kinases