Postdoc/Staff Scientist position in Structural Biology (biomolecular crystallography) at the Medical University Innsbruck (Austria) [Chiffre: MEDI-15891]

A university assistant (postdoc/staff scientist) position is available at the Institute of Biological Chemistry (chair: Prof. Klaus Scheffzek) in the Biocenter of the Medical University Innsbruck (Austria), salary scheme is B1, GH3, according to collective agreements (‘Kollektivvertrag’) for university employees.

Research in the laboratory focuses on mechanisms of signal regulation involving processes of medical relevance and on disease proteins.

Innsbruck is the capital of the Austrian state Tyrol with high quality of life and is a holiday place for people from all over the world. The institute is part of the Biocenter and is located in our new research building ‘Center for Chemistry and Biomedicine’ located at the river Inn. We have state of the art equipment to perform all steps from protein expression to structure determination by X-ray crystallography. These include prokaryotic and eukaryotic cell culture, several FPLCs for protein purification, a robotic crystallization screening and imaging laboratory as well as a separate hands-on crystallization lab. We have a Bruker-Microstar X-ray generator and regular access to beam time at the ESRF (Austrian BAG proposal).

The successful candidate will participate in and support structural biology/biochemical research in our institute. We are looking for a highly motivated scientist who likes to work in and contribute to an interdisciplinary structural biology environment tackling challenging projects involving signaling and disease proteins, among others. A Ph.D. in biochemistry, biophysics, physics, molecular biology or a related discipline is required. The ideal candidate has several years of research experience in an international laboratory using structural biology/crystallography and biochemical approaches to investigate mechanistic aspects of cellular processes, relevant to human health and disease. Specifically, experience in molecular biology, heterologous protein expression in prokaryotic/eukaryotic cells and purification are required. Proven experience in biomolecular structure determination by X-ray crystallography is of great advantage. Applicants are ideally able to supervise (under)graduate students and participate in university teaching.

Recent highlights of the laboratory include de Araujo et al. (2017), Science 358, 377; Dunzendorfer-Matt et al. (2016), PNAS 113, 7497.

Start: as soon as possible

Location: Medical University, CCB-Biocenter, Division of Biological Chemistry, Innrain 80-82

Contract: A contract for 4 years will be offered to the successful candidate. This can be renewed depending on review.

Innsbruck Medical University encourages explicitly application of qualified female candidates.

Salary: The current monthly salary is €3711.20 brutto (14x per year), salary scheme B1, GH3 (according to ‘Kollektivvertrag’).

Informal inquiries:

Applications should be sent by 11th April 2018 to

Application details:

  • Cover letter
  • CV
  • List of publications
  • Research summary incl. professional experience and interests
  • Contact information of 3 potential referees

PhD position, Medical University of Innsbruck, CCB-Biocenter/Division of Biological Chemistry, PI: Klaus Scheffzek

A PhD position in the structural biology of signal regulation by the Neurofibromatosis Type 1 (NF1) protein (for overview see: Ratner & Miller, 2015, Nat Rev Cancer. 15, 290-301) is available at the Division of Biological Chemistry of the Biocenter at Innsbruck Medical University.

Background: The project is about the 3D-characterization of a recently identified protein complex (Dunzendorfer et al., 2016, PNAS 113, 7497-7502; Stowe et al., 2012, Genes & Development 26, 1421-1426) employing biomolecular crystallography, biochemistry and potentially cell biology.

Funding is available for initially 3 years. Salary is according to the fwf-salary scheme. The successful candidate will be member of our Molecular Cell Biology and Oncology (MCBO) graduate program ( For inquiries/application please contact: Klaus.Scheffzek[at] Evaluation of applications will start April 10, 2017 and continue until the position is filled.

PhD position, Medical University of Innsbruck, CCB-Biocenter/Division of Cell Biology, PI: David Teis

A PhD Position is available immediately in the ‘Membrane Traffic and Signaling’ research group, Division of Cell Biology (http://www.i- at the BIOCENTER @ Innsbruck Medical University, Innsbruck, Austria (

Background: The uptake of glucose, amino acids and nucleobases via nutrient transporters is essential for controlled cell growth and survival. How these processes are regulated in response to changes in the extracellular environment is poorly characterized.

The goal of the thesis is to identify the ‘Molecular mechanism of nutrient dependent plasma membrane remodeling’. We have recently shown that nutrient limitation induces global but selective remodeling of the plasma membrane proteome in yeast, including the lysosomal degradation of many different nutrient transporters. This process cooperates with autophagy in a catabolic cascade that mediates entry into quiescence and is required to survive nutrient limitation (Mueller et al., eLife 2015).

Methods used: Now we aim to characterize how cellular homeostasis and signaling networks regulate the ubiquitin dependent degradation of nutrient transporters. Therefore we will combine yeast genetics with quantitative proteomics and imaging approaches. Our results will help to understand how cells adjust their nutrient transporter repertoire on the cell surface in response to nutrient availability and thus have important general biological implications for the regulation of cellular growth.

Requirements: Applicants should be highly motivated, with a strong background in cell- and molecular biology and/or biochemistry.

Please send your application (CV and two contacts for reference) per email to David Teis (


  1. Huber, L.A., and Teis, D. (2016). Lysosomal signaling in control of degradation pathways. Curr Opin Cell Biol 39, 8-14.
  2. Muller, M.*, Schmidt, O.*, Angelova, M., Faserl, K., Weys, S., Kremser, L., Pfaffenwimmer, T., Dalik, T., Kraft, C., Trajanoski, Z., Lindner H.H. and Teis, D. (2015). The coordinated action of the MVB pathway and autophagy ensures cell survival during starvation. eLife 4.
  3. Adell, M.A.*, Vogel, G.F.*, Pakdel, M., Muller, M., Lindner, H., Hess, M.W., and Teis, D. (2014). Coordinated binding of Vps4 to ESCRT-III drives membrane neck constriction during MVB vesicle formation. J Cell Biol 205, 33-49.

Master thesis project in the Division of Cell Biology, Teis-Lab, Biocenter, Medical University of Innsbruck.

Molecular Mechanism of starvation induced endocytosis
Growth factor receptors and nutrient transporters in the plasma membrane (PM) of eukaryotic cells play a critical role in cell growth, differentiation, and survival. Their selective ubiquitin dependent removal from the PM helps cells to properly adapt to changes in the extracellular environment. The molecular mechanisms underlying the endocytosis of activated growth factor receptors are well understood. In contrast, little is know how cells control and regulate the abundance of nutrient transporters. Our recent results shown, that nutrient limitation induces selective endocytosis and degradation of many different nutrient transporters. This starvation-induced endocytosis of nutrient transporters together with autophagy is required for cell survival during nutrient limitation (Müller, Schmidt et al. eLife 2015). Our finding implicate new regulatory mechanisms for endocytosis and we have identified the first key molecules that are required for this process.

In this Master-thesis project, you will work in a team that aims to understand the molecular mechanism driving starvation-induced endocytosis.

To do so, you will learn how to use live cell imaging imaging and biochemical approaches in combination with genetic approaches in yeast. The goal of this master-thesis project is to define the mechanistic concept in which cellular starvation program communication with the endocytic machinery and thereby survive nutrient limitation. The results obtained could have general implications on our understanding of how cells cope with nutrient stresses, and will unravel mechanisms likely to be of prime importance in many pathologies, including metabolic diseases and cancer.

Requirements: high level of motivation to solve basic cell biological problems
Start: the sooner the better
If you are interested please contact: