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Dr.
Burger-Kentischer, Anke
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PublicationControlled cell attachment, using plasma deposited polymer microstructures: A novel study of cells-substrate interactions( 2006)Several actual developments in medical therapy are focussing on the potential of a surface-dependent selection 1 and proliferation of special cell types. For an improvement of biocompatibility it is interesting to understand the interactions between cells and material surfaces in order to create devices with the respective characteristics. In this paper the possibility to isolate three different tumor cells lines are studied: HEK293, RINm5f and KYM-1. A procedure by means of plasma polymerization is demonstrated to create hydrophilic microstructures (precursor: AAc) on a hydrophobic (precursor: CHF3) substrate and shown to effectively select RINm5f cells. Moreover, by studying the interaction between culture media and deposited polymers, it is shown that Ca2+ ions and protein adsorption play a fundamental role in the cell-substrate adhesion and proliferation.
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PatentZellulärer Pyrogentest( 2006)
;Finkelmeier, D.(A1) Die Erfindung betrifft ein Verfahren, Mittel und Kits zum qualitativen und quantitativen Nachweis und Identifikation von Erregern und Erregerspektren auf Basis von Endotoxinen und anderen Pyrogenen. -
PublicationReduction of the aortic inflammatory response in spontaneous atherosclerosis by blockade of macrophage migration inhibitory factor (MIF)( 2006)
;Göbel, H. ;Zernecke, A. ;Bucala, R. ;Leng, L. ;Schaefer, H.E. ;Schober, A. ;Rütten, H. ;Ihling, C. -
PublicationIntracellular action of the cytokine MIF to modulate AP-1 activity and the cell cycle through Jab1( 2000)
;Hausser, A. ;Flieger, O. ;Roger, T. ;Calandra, T. ;Kapurniotu, A. ;Grell, M.Cytokines are multifunctional mediators that classically modulate immune activity by receptor-mediated pathways. Macrophage migration inhibitory factor (MIF) is a cytokine that has a critical role in several inflammatory conditions but that also has endocrine and enzymatic functions. The molecular targets of MIF action have so far remained unclear. Here we show that MIF specifically interacts with an intracellular protein, Jab1, which is a coactivator of AP-1 transcription that also promotes degradation of the cyclin-dependent kinase inhibitor p27(exp Kip1) (ref. 10). MIF colocalizes with Jab1 in the cytosol, and both endogenous and exogenously added MIF following endocytosis bind Jab 1. MIF inhibits Jab1- and stimulus-enhanced AP-1 activity; but does not interfere with the induction of the transcription factor NF(kappa)B. Jab1 activates c-Jun amino-terminal kinase (INK) activity and enhances endogenous phospho-c-Jun levels, and MIF inhibits these effects. MIF also antagonizes Jab1-dependent cell-cycle regulatioft by increasing p27(exp Kip1) expression through stabilization of p27(exp Kip1) protein. Consequently, Jab1-mediated rescue of fibroblasts from growth arrest is blocked by MIF Amino acids 50-65 and Cys 60 of MIF are important for Jab1 binding and modulation. We conclude that MIF may act broadly no negatively regulate Jab1-controlled pathways and that the MIF-Jab1 interaction may provide a molecular basis for key activities of MIF.