Lecturer

Johann Rotheneder

Teaching Statement

My aim in teaching is to facilitate the aquisition of knowledge as a basis for further learning and thinking. My teaching comprises lectures in Chemistry, Biochemistry, Molecular Biology, and Biostatistics for undergraduate medical students as well as specialized topics for medical and biology graduate students. I frequently integrate questions, procedures and results (including failures and mistakes) of my own research into my lectures. In laboratory courses students must understand not only the methods but also the principles and mechanisms underlying the question addressed in an experiment. I tell them my expectations of the contents of laboratory reports and provide them with well written examples. I consider these reports an opportunity for the students to improve their writing skills.

Scientific Statement

The mechanisms controlling growth and cell cycle are essential for the mammalian cell. Perturbations like DNA damage result in cell cycle arrest, senescence, or apoptosis. Dysfunction of these mechanisms often give rise to cancer. Involved in these processes on different levels is a protein called EAPP (E2F Associated PhosphoProtein) that we have identified and characterized. Tumor cells often overex-press EAPP, indicating that it confers a selective advantage to these cells. EAPP levels increase upon DNA damage and higher EAPP levels protect cells from apoptosis. Scrutinizing the function of EAPP is currently our main goal.

Biography

Johann Rotheneder studied Biochemistry at the University of Vienna, Austria and obtained a PhD at the Institute of Molecular Biology in Vienna where he continued as a postdoctoral fellow. In 2002 he became tenured as an Associate Professor at the Department of Medical Biochemistry of the Medical University of Vienna.

Spotlights

EAPP stimulates E2F-dependent transcription

We identified EAPP in a yeast two-hybrid screen for E2F1-interacting proteins. It also interacts with E2F2 and E2F3a, the other activating members of the E2F family of transcription factors. These interactions result in elevated E2F-dependent transcription.

EAPP levels determine cell fate during stress

Overexpression of EAPP results in cell cycle arrest. This is mediated by the cdk inhibitor p21. We could show that EAPP associates with the p21 promoter and is required for the assembly of the transcription pre-initiation complex. EAPP levels increase upon cellular stress resulting in elevated p21 which is anti-apoptotic. Lower EAPP thus facilitates, higher EAPP prevents apoptosis.

Checkpoint recovery after DNA double strand break repair is influenced by EAPP

DNA double strand breaks result in rapid activation of Chk2. This kinase phosphorylates and inactivates cdc25C, a phosphatase required for entry of mitosis. After repair of the breaks Chk2 has to be inactivated to allow continuation of the cell cycle. We showed that EAPP specifically binds phosphorylated Chk2 and this results in its inactivation by the recruitment of specific phosphatases.

    Selected Publications

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