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Research
Cell Cycle and Cell Proliferation
at the Biocenter, Area Biochemistry and Chemistry, Innsbruck
Research Leader: Dr. Ludger Hengst
Daniela Höller
Innsbruck Medical University, Biocenter, Medical Biochemistry, Fritz-Pregl-Str. 3, A-6020 Innsbruck
E-mail: Daniela.hoeller@i-med.ac.at
Phone: 0043-(0)512-9003-70 114 Fax: 0043-(0)512-9003-70115
Education and positions:
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EMBO long-term fellow with Prof. Ludger Hengst, Institute of Medical Biochemistry, Biocenter Innsbruck, Austria |
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Postdoctoral fellow with Prof. Ivan Dikic, Institute of Biochemistry II, Medical School, Goethe University, Frankfurt, Germany |
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PhD work at the Institute for Experimental Genetics (GSF); Supervisor PD Dr. Jerzy Adamski: „Regulation of Sonic Hedgehog signalling by Cholesterol“ |
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University studies: Food Chemistry, Technische Universität München |
Bibliography
Original articles:
- Raguz J, Wagner S, Dikic I, Hoeller D. Suppressor of T-cell receptor signalling 1 and 2 differentially regulate endocytosis and signalling of receptor tyrosine kinases. FEBS Lett. 2007 Oct 2;581(24):4767-72.
- Hoeller D*, Hecker C*, Wagner S, Dikic I. E3-independent self-ubiquitination of ubiquitin binding proteins. Mol Cell 2007 Jun 22;26(6):891-8.
- Hoeller D, Crosetto N, Blagoev B, Raiborg C, Tikkanen R, Wagner S, Kowanetz K, Breitling R, Mann M, Stenmark H, Dikic I. Regulation of ubiquitin-binding proteins by monoubiquitylation. Nat Cell Biol. 2006 Feb, 8(2):163-169.
- Jozic D, Cardenes N, Deribe YL, Moncalian G, Hoeller D, Groemping Y, Dikic I, Rittinger K, Bravo J. Cbl promotes clustering of endocytic adaptor proteins. Nat Struct Mol Biol. 2005 Oct; 9(12):972-979
- Schmidt MH, Höller D, Yu J, Furnari FB, Cavenee WK, Dikic I, Bogler O. Alix/AIP1 antagonizes epidermal growth factor receptor downregulation by the Cbl-SETA/CIN85 complex. Mol Cell Biol. 2004 Oct; 24(20):8981-93.
- Kowanetz K, Husnjak K, Höller D, Kowanetz M, Soubeyran P, Hirsch D, Schmidt MH, Pavelic K, De Camilli P, Randazzo PA, Dikic I. CIN85 associates with multiple effectors controlling intracellular trafficking of epidermal growth factor receptors.Mol Biol Cell. 2004 Jul;15(7):3155-66.
- Breitling R, Laubner D, Clizbe D, Adamski J, Krisans SK. Isopentenyl-diphosphate isomerases in human and mouse: evolutionary analysis of a mammalian gene duplication. J Mol Evol. 2003 Sep; 57(3):282-91.
- Marijanovic Z*, Laubner D*, Moller G, Gege C, Husen B, Adamski J, Breitling R. Closing the gap: identification of human 3-ketosteroid reductase, the last unknown enzyme of mammalian cholesterol biosynthesis. Mol Endocrinol. 2003 Sep;17(9):1715-25.
- Laubner D, Breitling R, Adamski J. Embryonic expression of cholesterogenic genes is restricted to distinct domains and colocalizes with apoptotic regions in mice. Mol Brain Res. 2003 Jul;115(1):87-92.
- Beer C, Buhr P, Hahn H, Laubner D, Wirth M. Gene expression analysis of murine cells producing amphotropic mouse leukaemia virus at a cultivation temperature of 32 and 37 degrees C. J Gen Virol. 2003 Jul; 84(7):1677-86.
- Breitling R, Laubner D, Adamski J. Structure-based phylogenetic analysis of short-chain alcohol dehydrogenases and reclassification of the 17beta-hydroxysteroid dehydrogenase family. Mol Biol Evol. 2001 Dec;18(12):2154-61.
* equally contributing authors
Review articles:
- Hoeller D, Hecker C, Dikic I. Ub and Ub-like proteins in cancer pathogenesis. Nat Rev Cancer. 2006 Oct; 10(6): 776-88
- Breitling R, Hoeller D. Current challenges in quantitative modeling of epidermal growth factor signaling. FEBS Letters. 2005 Nov; 579(28):6289-94
- Höller D, Volarevic S, Dikic I. Compartmentalization of growth factor receptor signalling. Curr Opin Cell Biol. 2005 April; 17(2):107-111
- Holler D and Dikic I. Receptor endocytosis via ubiquitin-dependent and -independent pathways. Biochem Pharmacol. 2004 Mar 15;67(6):1013-7.
Current research interest:
Cell cycle progression is a fundamental biological process that relies on the ordered activation and inactivation of distinct cyclin-dependent kinases (Cdks). The Cdk inhibitor p27 is a key regulator of Cdk activity during quiescence and in G1. Deregulation of p27 has been associated with increased tumor malignancy and poor prognosis in individuals with various types of cancer. p27 protein is abundant in quiescent cells. Mitogen-induced phosphorylation of p27 is linked to ubiquitin-dependent degradation of the inhibitor in G1-phase and consequently allows cells to progress into S-phase. Tyrosine phosphorylation of p27 by Src family kinases or Bcr-Abl links cell cycle control directly to RTK signalling. There are at least seven phosphorylation sites present in p27 raising the questions of how they are coordinated/regulated in space and time to ensure proper function of the protein. Besides the Cdk-related functions, very little is known about signals that modify p27 triggering the formation of complexes that are responsible for Cdk-independent processes such as apoptosis or cell motility.
Although phosphorylation of p27 has been extensively studied, little is known about the timing and interplay of the different modifications during cell cycle progression, and how they impinge on Cdk-dependent and potential Cdk-independent functions of p27. I would like to get a qualitative and quantitative insight into the spectrum and dynamics of post-translational p27 modifications including phosphorylation, ubiquitylation, sumoylation and acetylation. Moreover, I am interested to understand how distinct modifications of p27 direct the assembly of specific p27-associated protein complexes in different cellular compartments and cell-cycle phases.
Open positions:
We are looking for highly motivated PhD students who are interested in molecular biology, cell signalling and cell cycle regulation to work on the above described topic. Please contact Prof. Ludger Hengst (ludger.hengst@i-med.ac.at) or myself (Daniela.hoeller@i-med.ac.at) for further information.