Version 2 2019-12-05, 17:12Version 2 2019-12-05, 17:12
Version 1 2019-11-18, 18:11Version 1 2019-11-18, 18:11
dataset
posted on 2019-12-05, 17:12authored byShaked Bar-Cohen, Navit Mooshayef, Rotem Lange, Allan Bar-Sinai, Helit Rozen, Adi Salzberg, David Engelberg, Ze’ev Paroush
Excessive RTK signaling,
often caused by activating mutations in Ras, Raf and/or MEK, occurs in most
human tumors. Intriguingly, confirmed cancer-driver mutations in the downstream
effector kinase, ERK, have not been reported. To test if active ERK mutants can
function as oncoproteins, we introduced an activating mutation, originally identified in a yeast ERK, into the single Drosophila ERK. We find that this mutation
renders ERK catalytically active independently of upstream signaling, and that its expression induces extensive
over-proliferation and hyperplastic tumor formation in vivo. Thus, some human ERK1/2 mutations identified in
patient-derived tumours may actually represent overlooked oncogenic, cancer-causing
mutations.
History
Article title
An Activating Mutation in ERK Causes Hyperplastic Tumors in a scribble Mutant Tissue in Drosophila