M. (Mario) Mauthe

Research

Publications
  1. The farnesyl transferase inhibitor lonafarnib inhibits mTOR signaling and enforces sorafenib-induced apoptosis in melanoma cells

    Niessner, H., Beck, D., Sinnberg, T., Lasithiotakis, K., Maczey, E., Gogel, J., Venturelli, S., Berger, A., Mauthe, M., Toulany, M., Flaherty, K., Schaller, M., Schadendorf, D., Proikas-Cezanne, T., Schittek, B., Garbe, C., Kulms, D. & Meier, F. Feb-2011 In : Journal of Investigative Dermatology. 131, 2, p. 468-479 12 p.

    Research output: Contribution to journalArticle

  2. Ca2+/calmodulin-dependent kinase (CaMK) signaling via CaMKI and AMP-activated protein kinase contributes to the regulation of WIPI-1 at the onset of autophagy

    Pfisterer, S. G., Mauthe, M., Codogno, P. & Proikas-Cezanne, T. Dec-2011 In : Molecular Pharmacology. 80, 6, p. 1066-1075 10 p.

    Research output: Contribution to journalArticle

  3. Modulation of glutamine metabolism by the PI(3)K-PKB-FOXO network regulates autophagy

    van der Vos, K. E., Eliasson, P., Proikas-Cezanne, T., Vervoort, S. J., van Boxtel, R., Putker, M., van Zutphen, I. J., Mauthe, M., Zellmer, S., Pals, C., Verhagen, L. P., Groot Koerkamp, M. J. A., Braat, A. K., Dansen, T. B., Holstege, F. C., Gebhardt, R., Burgering, B. M. & Coffer, P. J. 14-Aug-2012 In : Nature Cell Biology. 14, 8, p. 829-837 9 p.

    Research output: Contribution to journalArticle

  4. Resveratrol-mediated autophagy requires WIPI-1-regulated LC3 lipidation in the absence of induced phagophore formation

    Mauthe, M., Jacob, A., Freiberger, S., Hentschel, K., Stierhof, Y-D., Codogno, P. & Proikas-Cezanne, T. 7-Dec-2011 In : Autophagy. 7, 12, p. 1448-1461 14 p.

    Research output: Contribution to journalArticle

  5. WIPI-1 Positive Autophagosome-Like Vesicles Entrap Pathogenic Staphylococcus aureus for Lysosomal Degradation

    Mauthe, M., Yu, W., Krut, O., Krönke, M., Götz, F., Robenek, H. & Proikas-Cezanne, T. 9-Jul-2012 In : International Journal of Cell Biology. 2012, p. 179207 14 p.

    Research output: Contribution to journalArticle

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