Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation

@inproceedings{Lochhead2016TumorCW,
  title={Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation},
  author={Pamela A. Lochhead and Jonathan J Clark and Lan-Zhen Wang and Lesley Gilmour and Matthew Squires and Rebecca Gilley and Caroline Foxton and David R. Newell and Stephen R. Wedge and Simon J Cook},
  booktitle={Cell cycle},
  year={2016}
}
ERK5, encoded by MAPK7, has been proposed to play a role in cell proliferation, thus attracting interest as a cancer therapeutic target. While oncogenic RAS or BRAF cause sustained activation of the MEK1/2-ERK1/2 pathway, ERK5 is directly activated by MEK5. It has been proposed that RAS and RAF proteins can also promote ERK5 activation. Here we investigated the interplay between RAS-RAF-MEK-ERK and ERK5 signaling and studied the role of ERK5 in tumor cell proliferation in 2 disease-relevant… CONTINUE READING
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