@article{BenzMerkelOffneretal.2013, author = {Benz, Peter M. and Merkel, Carla J. and Offner, Kristin and Abeßer, Marco and Ullrich, Melanie and Fischer, Tobias and Bayer, Barbara and Wagner, Helga and Gambaryan, Stepan and Ursitti, Jeanine A. and Adham, Ibrahim M. and Linke, Wolfgang A. and Feller, Stephan M. and Fleming, Ingrid and Renn{\´e}, Thomas and Frantz, Stefan and Unger, Andreas and Schuh, Kai}, title = {Mena/VASP and alphaII-Spectrin complexes regulate cytoplasmic actin networks in cardiomyocytes and protect from conduction abnormalities and dilated cardiomyopathy}, series = {Cell Communication and Signaling}, volume = {11}, journal = {Cell Communication and Signaling}, number = {56}, doi = {10.1186/1478-811X-11-56}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128760}, year = {2013}, abstract = {Background: In the heart, cytoplasmic actin networks are thought to have important roles in mechanical support, myofibrillogenesis, and ion channel function. However, subcellular localization of cytoplasmic actin isoforms and proteins involved in the modulation of the cytoplasmic actin networks are elusive. Mena and VASP are important regulators of actin dynamics. Due to the lethal phenotype of mice with combined deficiency in Mena and VASP, however, distinct cardiac roles of the proteins remain speculative. In the present study, we analyzed the physiological functions of Mena and VASP in the heart and also investigated the role of the proteins in the organization of cytoplasmic actin networks. Results: We generated a mouse model, which simultaneously lacks Mena and VASP in the heart. Mena/VASP double-deficiency induced dilated cardiomyopathy and conduction abnormalities. In wild-type mice, Mena and VASP specifically interacted with a distinct αII-Spectrin splice variant (SH3i), which is in cardiomyocytes exclusively localized at Z- and intercalated discs. At Z- and intercalated discs, Mena and β-actin localized to the edges of the sarcomeres, where the thin filaments are anchored. In Mena/VASP double-deficient mice, β-actin networks were disrupted and the integrity of Z- and intercalated discs was markedly impaired. Conclusions: Together, our data suggest that Mena, VASP, and αII-Spectrin assemble cardiac multi-protein complexes, which regulate cytoplasmic actin networks. Conversely, Mena/VASP deficiency results in disrupted β-actin assembly, Z- and intercalated disc malformation, and induces dilated cardiomyopathy and conduction abnormalities.}, language = {en} } @article{CzerniukBrueggemannTepperetal.2014, author = {Czerniuk, T. and Br{\"u}ggemann, C. and Tepper, J. and Brodbeck, S. and Schneider, C. and Kamp, M. and H{\"o}fling, S. and Glavin, B. A. and Yakovlev, D. R. and Akimov, A. V. and Bayer, M.}, title = {Lasing from active optomechanical resonators}, series = {Nature Communications}, volume = {5}, journal = {Nature Communications}, doi = {10.1038/ncomms5038}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-121559}, pages = {4038}, year = {2014}, abstract = {Planar microcavities with distributed Bragg reflectors (DBRs) host, besides confined optical modes, also mechanical resonances due to stop bands in the phonon dispersion relation of the DBRs. These resonances have frequencies in the 10- to 100-GHz range, depending on the resonator's optical wavelength, with quality factors exceeding 1,000. The interaction of photons and phonons in such optomechanical systems can be drastically enhanced, opening a new route towards the manipulation of light. Here we implemented active semiconducting layers into the microcavity to obtain a vertical-cavity surface-emitting laser (VCSEL). Thereby, three resonant excitations--photons, phonons and electrons--can interact strongly with each other providing modulation of the VCSEL laser emission: a picosecond strain pulse injected into the VCSEL excites long-living mechanical resonances therein. As a result, modulation of the lasing intensity at frequencies up to 40 GHz is observed. From these findings, prospective applications of active optomechanical resonators integrated into nanophotonic circuits may emerge.}, language = {en} } @article{SchneiderSchauliesSchneiderSchauliesSchusteretal.1994, author = {Schneider-Schaulies, Sibylle and Schneider-Schaulies, J{\"u}rgen and Schuster, A. and Bayer, M. and Pavlovic, J. and ter Meulen, V.}, title = {Cell type specific MxA-mediated inhibition of measles virus transcription in human brain cells}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-62255}, year = {1994}, abstract = {No abstract available}, subject = {Virologie}, language = {en} } @article{SchneiderSchauliesSchneiderSchauliesSchusteretal.1994, author = {Schneider-Schaulies, J{\"u}rgen and Schneider-Schaulies, S. and Schuster, A. and Bayer, M. and Pavlovic, J. and ter Meulen, V.}, title = {Cell type specific MxA-mediated inhibition of measles virus transcription in human brain cells}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34313}, year = {1994}, abstract = {Measles virus (MV)-specific transcription in human brain cells is characterized by particularly low abundances of the distal mRNAs encoding the MV envelope proteins. Similar transcriptional restrictions of the closely related vesicular stomatitis virus have been observed in mouse fibroblasts constitutively expressing the interferon-inducible MxA protein (P. Staeheli and J. Pavlovic, J. Virol. 65:4498-4501, 1991). We found that MV infection of human brain cells is accompanied by rapid induction and high-level expression of endogenous MxA proteins. After stable transfection of MxA, human glioblastoma cells (U-87-MxA) released 50- to 100-fold less infectious virus and expression of viral proteinswas highly restricted. The overall MV-specific transcription Ievels were reduced by up to 90\%, accompanied by low relative frequencies of the distal MV-specific mRNAs. These restrictions were linked to an inhibition of viral RNA synthesis and not to a decreased stability of the viral RNAs. Our results indicate that expression of MxA is associated with transcriptional attenuation of MV in brain cells, thus probably contributing to the establishment of persistent MV central nervous system infections. In addition, the mechanism of MxA-dependent resistance against MV infection, in contrast to that of vesicular Stomatitis virus, is cell type specific, because an inhibition of MV glycoprotein synthesis independent of transcriptional alterations was observed in MxA-transfected human monocytes}, language = {en} } @article{SchneiderSchauliesSchneiderSchauliesBayeretal.1993, author = {Schneider-Schaulies, Sibylle and Schneider-Schaulies, J{\"u}rgen and Bayer, M. and L{\"o}ffler, S. and ter Meulen, V.}, title = {Spontaneous and differentiation dependent regulation of measles virus gene expression in human glial cells}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54913}, year = {1993}, abstract = {The expression of measles virus (MV) in six different permanent human glioma cell lines (D-54, U-251, U-138, U-105, U-373, and D-32) was analyzed. Although all celllines were permissive for productive replication of all MV strains tested, U-251, D-54, and D-32 cells spontaneously revealed restrictions of MV transcription similar to those observed for primary rat astroglial cells and brain tissue. In vitro differentiation of D-54 and U-251 cells by substances affecting tbe intracellular cyclic AMP Ievel caused a significant reduction of tbe expression of tbe viral proteins after 18, 72, and 144 b of infection. This pronounced restriction was not paralleled to a comparable Ievel by an inhibition of tbe syntbesis and biological activity in vitro of virus·specific mRNAs as sbown by quantitative Northem (RNA) blot analyses and in vitro translation. The block in viral protein syntbesis could not be attributed to tbe induction of type I interferon by any of tbe substances tested. Our findings indicate tbat down-regulation of MV gene expression in human brain cells can occur by a cell type-rlependent regulation of tbe viral mRNA transcription and a differentiation-dependent regulation of translation, botb of wbicb may be crucial for the establisbment of persistent MV infections in tbe centrat nervous system.}, subject = {Immunologie}, language = {en} } @article{JahnkeGiesAssmannetal.2016, author = {Jahnke, Frank and Gies, Christopher and Aßmann, Marc and Bayer, Manfred and Leymann, H.A.M. and Foerster, Alexander and Wiersig, Jan and Schneider, Christian and Kamp, Martin and H{\"o}fling, Sven}, title = {Giant photon bunching, superradiant pulse emission and excitation trapping in quantum-dot nanolasers}, series = {Nature Communications}, volume = {7}, journal = {Nature Communications}, number = {11540}, doi = {10.1038/ncomms11540}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166144}, year = {2016}, abstract = {Light is often characterized only by its classical properties, like intensity or coherence. When looking at its quantum properties, described by photon correlations, new information about the state of the matter generating the radiation can be revealed. In particular the difference between independent and entangled emitters, which is at the heart of quantum mechanics, can be made visible in the photon statistics of the emitted light. The well-studied phenomenon of superradiance occurs when quantum-mechanical correlations between the emitters are present. Notwithstanding, superradiance was previously demonstrated only in terms of classical light properties. Here, we provide the missing link between quantum correlations of the active material and photon correlations in the emitted radiation. We use the superradiance of quantum dots in a cavity-quantum electrodynamics laser to show a direct connection between superradiant pulse emission and distinctive changes in the photon correlation function. This directly demonstrates the importance of quantum-mechanical correlations and their transfer between carriers and photons in novel optoelectronic devices.}, language = {en} }