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Max-Planck-Institute of Molecular Biomedicine in Muenster, Germany Postdoc募集

A postdoctoral position is immediately available at the department of vascular cell biology (http://www.mpi-muenster.mpg.de/nvz/puble.shtml) at the Max-Planck-Institute of Molecular Biomedicine in Muenster. We study the molecular and cellular mechanisms of leukocyte trafficking and extravasation in inflammation and lymphocyte homing. In this context we focus on the regulation of endothelial cell contacts during transmigration of lymphocytes. This topic is addressed by all modern cell biological and immunological techniques as well as by generating and analyzing transgenic knock-in and knock-out mice. A second topic in the lab deals with the role of endothelial cell contact plasticity in angiogenesis.

We seek highly qualified and motivated coworkers with training in biology, cell biology, biochemistry or immunology. Experience in vascular biology would be welcome but is not a requirement.

Further questions and applications (preferentially in electronic form) with curriculum vitae, a short description of research interest and names/addresses of referees should be sent to:
Prof. Dr. Dietmar Vestweber
Max-Planck-Institute of Molecular Biomedicine
Roentgen Str. 20, 48149 Muenster, Germany
vestweb@mpi-muenster.mpg.de

Selected recent publications:

Nottebaum AF, Cagna G, Winderlich M, Gamp AC, Linnepe R, Polaschegg C, Filippova K, Lyck R, Engelhardt B, Kamenyeva O, Bixel MG, Butz S, Vestweber D. VE-PTP maintains the endothelial barrier via plakoglobin and becomes dissociated from VE-cadherin by leukocytes and by VEGF. J. Exp. Med. 205: 2929-2945 (2008)
Saharinen P, Eklund L, Miettinen J, Wirkkala R, Anisimov A, Winderlich M, Nottebaum A, Vestweber D, Deutsch U, Koh GY, Olsen BR, Alitalo K. Angiopoietins assemble distinct Tie2 signalling complexes in endothelial cell-cell and cell-matrix contacts. Nat. Cell Biol. 10:527-537 (2008)
Bixel MG, Petri B, Khandoga AG, Khandoga A, Wolburg-Buchholz K, Wolburg H, Marz S, Krombach F, Vestweber D. A CD99-related antigen on endothelial cells mediates neutrophil, but not lymphocyte extravasation. Blood 109: 5327-5336 (2007
Wegmann F, Petri J, Khandoga AG, Moser C, Khandoga A, Volkery S, Li H, Nasdala I, Brandau O, Fässler R, Butz S, Krombach F, Vestweber D. ESAM supports neutrophil extravasation, activation of Rho and VEGF-induced vascular permeability. J. Exp. Med. 203:1671-1677 (2006)

Posted by Prof. Dr. Dietmar Vestweber (vestweb@mpi-muenster.mpg.de)

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