Olson Eric N
Department of Molecular Biology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9148, USA.
J Clin Invest. 2004 Apr;113(8):1110-2. doi: 10.1172/JCI21497.
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.
众多刺激可激活大丝裂原活化蛋白激酶1（BMK1），这是一种能激活肌细胞增强因子2（MEF2）转录因子的丝裂原活化蛋白激酶。条件性基因缺失表明BMK1是内皮细胞存活所必需的。活性形式的MEF2C可部分绕过体外内皮细胞存活对BMK1的需求。这些发现揭示了BMK1 - MEF2信号在内皮细胞存活途径中的重要作用，并引发了关于这种反应分子基础的有趣问题。
