New regulatory mechanisms of G protein-mediated ERK1/2 activation in cardiovascular cells
K. Lorenz, M. Lohse
We have discovered a new regulatory mechanism of the extracellular kinases 1 and 2 (ERK1/2), which plays an essential role in ERK1/2 mediated cardiac hypertrophy. The mechanism is dependent on G proteins and the canonical ERK1/2 activation (phosphorylation of the TEY motif) and leads to Thr188 autophosphorylation of ERK1/2. ERKThr188 phosphorylation promotes nuclear localization of ERK and the activation of nuclear ERK substrates. We have started to investigate this mechanism and its regulation in detail and want to understand its physiological effects in the different cell types of the cardiovascular system by analyzing isolated cells and transgenic mouse models.