Anne Dwertmann

Publications

• 9.58

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  The Arf tumor suppressor protein inhibits Miz1 to suppress cell adhesion and induce apoptosis.

  Barbara Herkert, Anne Dwertmann, Steffi Herold, Mona Abed, Jean-Francois Naud, Florian Finkernagel, Gregory S Harms, Amir Orian, Michael Wanzel, Martin Eilers

  The Journal of cell biology. 03/2010; 188(6):905-18.

  Oncogenic stress induces expression of the alternate reading frame (Arf) tumor suppressor protein. Arf then stabilizes p53, which leads to cell cycle arrest or apoptosis. The mechanisms that distinguish both outcomes are incompletely understood. In this study, we show that Arf interacts with the Myc... [more] Oncogenic stress induces expression of the alternate reading frame (Arf) tumor suppressor protein. Arf then stabilizes p53, which leads to cell cycle arrest or apoptosis. The mechanisms that distinguish both outcomes are incompletely understood. In this study, we show that Arf interacts with the Myc-associated zinc finger protein Miz1. Binding of Arf disrupts the interaction of Miz1 with its coactivator, nucleophosmin, induces the sumoylation of Miz1, and facilitates the assembly of a heterochromatic complex that contains Myc and trimethylated H3K9 in addition to Miz1. Arf-dependent assembly of this complex leads to the repression of multiple genes involved in cell adhesion and signal transduction and induces apoptosis. Our data point to a tumor-suppressive pathway that weakens cell-cell and cell-matrix interactions in response to expression of Arf and that may thereby facilitate the elimination of cells harboring an oncogenic mutation.

• The Arf tumor suppressor protein antagonizes Miz1 function to suppress cell adhesion and induce apoptosis

  Anne Dwertmann, Barbara Herkert, Michael Wanzel, Steffi Herold, Florian Finkernagel, Martin Eilers

  EMBL PhD Symposium 2009, EMBO, Heidelberg, Germany; 01/2009

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