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Tunneling Anisotropic Magnetoresistance in Multilayer-(Co/Pt)/AlOx/PtStructures
Park, B. G.,Wunderlich, J.,Williams, D. A.,Joo, S. J.,Jung, K. Y.,Shin, K. H.,Olejní,k, K.,Shick, A. B.,Jungwirth, T. American Physical Society 2008 Physical Review Letters Vol.100 No.8
<P>We report observations of tunneling anisotropic magnetoresitance (TAMR) in vertical tunnel devices with a ferromagnetic multilayer-(Co/Pt) electrode and a nonmagnetic Pt counterelectrode separated by an AlOx barrier. In stacks with the ferromagnetic electrode terminated by a Co film the TAMR magnitude saturates at 0.15% beyond which it shows only weak dependence on the magnetic field strength, bias voltage, and temperature. For ferromagnetic electrodes terminated by two monolayers of Pt we observe order(s) of magnitude enhancement of the TAMR and a strong dependence on field, temperature and bias. The discussion of experiments is based on relativistic ab initio calculations of magnetization orientation dependent densities of states of Co and Co/Pt model systems.</P>
Claudia Dafinger,Markus M. Rinschen,Lori Borgal,Carolin Ehrenberg,Sander G. Basten,Mareike Franke,Martin Höhne,Manfred Rauh,Heike Göbel,Wilhelm Bloch,F. Thomas Wunderlich,Dorien J. M. Peters,Dirk Tasch 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Ciliopathies comprise a large number of hereditary human diseases and syndromes caused by mutations resulting in dysfunction of either primary or motile cilia. Both types of cilia share a similar architecture. While primary cilia are present on most cell types, expression of motile cilia is limited to specialized tissues utilizing ciliary motility. We characterized protein complexes of ciliopathy proteins and identified the conserved AAA-ATPase Ruvbl1 as a common novel component. Here, we demonstrate that Ruvbl1 is crucial for the development and maintenance of renal tubular epithelium in mice: both constitutive and inducible deletion in tubular epithelial cells result in renal failure with tubular dilatations and fewer ciliated cells. Moreover, inducible deletion of Ruvbl1 in cells carrying motile cilia results in hydrocephalus, suggesting functional relevance in both primary and motile cilia. Cilia of Ruvbl1-negative cells lack crucial proteins, consistent with the concept of Ruvbl1-dependent cytoplasmic pre-assembly of ciliary protein complexes.