Supplemental Material for Kushnir et al., 2020
Datasets usually provide raw data for analysis. This raw data often comes in spreadsheet form, but can be any collection of data, on which analysis can be performed.
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.