[Sweden] Postdoctoral Position University of Gothenburg
Postdoctoral position open in the field of cell adhesion and its regulation by intracellular signalling.
Estimated starting date: beginning of 2008.
Our research group is focusing on the consequences of signalling from c-erbB2, a receptor tyrosine kinase subunit and proto-oncogene involved in aggressive breast cancer, on the function of cell adhesion molecules, especially integrins, in mammary epithelial
cells. We have established a model system in which mammary epithelial cells are subjected to c-erbB2 signalling for various durations and then analysed with respect to intracellular signalling events, morphogenesis, adhesion and integrin conformation. Using this system,
we have identified a erbB2-induced mechanism for integrin inactivation which is dependent on signalling molecules such as MEK, Rho, PKB and integrin-linked kinase (ILK). Our present efforts are mainly focused at the role of ILK in integrin regulation and also at the mechanism of c-erbB2-induced ILK activation. To this end we use techniques such as RNAi, phosphoprotein analysis, flow cytometry-based measurements of integrin conformation, mass s!
pectrometry-assisted proteomics and phosphoproteomics, confocal techniques, as well as cell-based assays for adhesion and morphogenesis.
There is also an interest in the mechanisms and consequences of c-erbB2-induced epithelial-mesenchymal transition and subsequent acquistion of anchorage-independent growth.
Relevant references are:
- Lindberg, L. E., Hedjazifar, S. and Baeckstrom, D. c-erbB2-induced disruption of matrix adhesion and morphogenesis reveals a novel role for protein kinase B as a negative regulator of alpha2beta1 integrin function. Mol. Biol. Cell, 13, 2895-2909 (2002).
- Hedjazifar, S., Jenndahl, L., Shimokawa, H. and Baeckstrom, D. PKB mediates c-erbB2-induced epithelial beta1 integrin inactivation through Rho-independent F-actin rearrangements. Exp. Cell Res.307, 259-275 (2005)
- Jenndahl, L., Isakson, P., and Baeckstrom, D. c-erbB2-induced epithelial-mesenchymal transition in mammary epithelial cells is suppressed by cell-cell contact and initiated prior to E-cadherin downregulation. Int. J. Oncol., 27, 439-448 (2005)
- Jenndahl, L. E., Taylor-Papadimitriou, J. and Baeckstrom, D. Characterisation of integrin- and anchorage-dependence in mammary epithelial cells following c-erbB2-induced epithelial-mesenchymal transition. Tumor Biol., 27, 50-58 (2006).
The successful applicant will have a background in intracellular signalling and/or cell adhesion, experience with cell culture work and with at least some of the techniques mentioned above, fluency in English and a PhD thesis based on accepted papers in international, peer-reviewed journals.
Please send applications, always including a full CV with publication list, to my email address: dan.baeckstrom@medkem.gu.se
Be sure to include the phrase “Postdoc 08″ in the subject heading of your email to ensure passage through spam filters.
Dan Baeckstrom, Ph D
Institute of Biomedicine, Department of Medical Biochemistry and Cell
Biology, The Sahlgrenska Academy at the University of Gothenburg
Postal address:Box 440, SE-405 30 Gothenburg, Sweden
Street address: Medicinaregatan 9A, Gothenburg, Sweden
email: dan.baeckstrom@medkem.gu.se
website: http://dan1.medkem.gu.se
