Springer Nature
Browse
12964_2016_128_MOESM3_ESM.pdf (27.7 MB)

Additional file 3: of Feedback activation of neurofibromin terminates growth factor-induced Ras activation

Download (27.7 MB)
journal contribution
posted on 2016-02-09, 05:00 authored by Anne Hennig, Robby Markwart, Katharina Wolff, Katja Schubert, Yan Cui, Ian Prior, Manuel Esparza-Franco, Graham Ladds, Ignacio Rubio
Combined knockdown of MEK1 and MEK2 causes prolonged Ras activation. EGF-induced Ras activation was assessed biochemically after single or combined siRNA-mediated knockdown of MEK1 and MEK2. RBD designates the coomassie-stained Ras binding domain used to collect Ras-GTP from cell lysates. Note that single knockdown of MEK1 or MEK2 leads to opposite effects on Ras-GTP levels, pointing to different roles of both kinases in Ras activity control. The same effect was previously reported by Kamioka et al. [13]. (PDF 28364 kb)

Funding

Deutsche Forschungsgemeinschaft

History

Usage metrics

    Cell Communication and Signaling

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC