TY - THES A1 - Reinke, Julia T1 - The Role of Kallistatin in Energy Metabolism and Glucose Homeostasis in Mice Y1 - 2016 ER - TY - THES A1 - Reeg, Sandra T1 - Degradation of oxidized proteins by the proteasome - Involvement of chaperones and the ubiquitin-system Y1 - 2016 ER - TY - THES A1 - Heinle, Karolin T1 - Identifizierung von Kohlenhydratbindungsstellen in β-Helix-Proteinen Y1 - 2016 ER - TY - THES A1 - Sviben, Sanja T1 - Calcite biomineralization in coccolithophores BT - new insights from ultrastructural and proteomic studies of Emiliania huxleyi Y1 - 2016 ER - TY - THES A1 - Klimczak, Franziska T1 - Bildlichkeit und Metaphorik in spätmittelalterlichen Fastnachtspielen des 15. Jahrhunderts BT - wie Sexualität von sich reden macht Y1 - 2016 ER - TY - THES A1 - Armarego-Marriott, Tegan T1 - From dark to light BT - an overexpression and systems biology approach to investigate the development of functional thylakoid membranes Y1 - 2016 ER - TY - JOUR A1 - Wisotzki, Lutz A1 - Bacon, Roland A1 - Blaizot, J. A1 - Brinchmann, Jarle A1 - Herenz, Edmund Christian A1 - Schaye, Joop A1 - Bouche, Nicolas A1 - Cantalupo, Sebastiano A1 - Contini, Thierry A1 - Carollo, C. M. A1 - Caruana, Joseph A1 - Courbot, J. -B. A1 - Emsellem, E. A1 - Kamann, S. A1 - Kerutt, Josephine Victoria A1 - Leclercq, F. A1 - Lilly, S. J. A1 - Patricio, V. A1 - Sandin, C. A1 - Steinmetz, Matthias A1 - Straka, Lorrie A. A1 - Urrutia, Tanya A1 - Verhamme, A. A1 - Weilbacher, Peter Michael A1 - Wendt, Martin T1 - Extended Lyman alpha haloes around individual high-redshift galaxies revealed by MUSE JF - Science N2 - We report the detection of extended Ly alpha emission around individual star-forming galaxies at redshifts z = 3-6 in an ultradeep exposure of the Hubble Deep Field South obtained with MUSE on the ESO-VLT. The data reach a limiting surface brightness (1 sigma) of similar to 1 x 10(-19) erg s(-1) cm(-2) arcsec(-2) in azimuthally averaged radial profiles, an order of magnitude improvement over previous narrowband imaging. Our sample consists of 26 spectroscopically confirmed Ly alpha-emitting, but mostly continuum-faint (m(AB) greater than or similar to 27) galaxies. In most objects the Ly alpha emission is considerably more extended than the UV continuum light. While five of the faintest galaxies in the sample show no significantly detected Ly alpha haloes, the derived upper limits suggest that this is due to insufficient S/N. Ly alpha haloes therefore appear to be ubiquitous even for low-mass (similar to 10(8)-10(9) M-circle dot) star-forming galaxies at z > 3. We decompose the Ly alpha emission of each object into a compact component tracing the UV continuum and an extended halo component, and infer sizes and luminosities of the haloes. The extended Ly alpha emission approximately follows an exponential surface brightness distribution with a scale length of a few kpc. While these haloes are thus quite modest in terms of their absolute sizes, they are larger by a factor of 5-15 than the corresponding rest-frame UV continuum sources as seen by HST. They are also much more extended, by a factor similar to 5, than Ly alpha haloes around low-redshift star-forming galaxies. Between similar to 40% and greater than or similar to 90% of the observed Ly alpha flux comes from the extended halo component, with no obvious correlation of this fraction with either the absolute or the relative size of the Ly alpha halo. Our observations provide direct insights into the spatial distribution of at least partly neutral gas residing in the circumgalactic medium of low to intermediate mass galaxies at z > 3. KW - galaxies: high-redshift KW - galaxies: evolution KW - galaxies: formation KW - cosmology: observations KW - intergalactic medium Y1 - 2016 U6 - https://doi.org/10.1051/0004-6361/201527384 SN - 1432-0746 VL - 587 PB - EDP Sciences CY - Les Ulis ER - TY - JOUR A1 - Steinmetz, Matthias T1 - Die Vermessung des Universums JF - Vision als Aufgabe : das Leibniz-Universum im 21. Jahrhundert Y1 - 2016 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:b4-opus4-25899 SN - 978-3-939818-67-0 SP - 197 EP - 210 PB - Berlin-Brandenburgische Akademie der Wissenschaften CY - Berlin ER - TY - JOUR A1 - Cui, Huanhuan A1 - Schlesinger, Jenny A1 - Schoenhals, Sophia A1 - Toenjes, Martje A1 - Dunkel, Ilona A1 - Meierhofer, David A1 - Cano, Elena A1 - Schulz, Kerstin A1 - Berger, Michael F. A1 - Haack, Timm A1 - Abdelilah-Seyfried, Salim A1 - Bulyk, Martha L. A1 - Sauer, Sascha A1 - Sperling, Silke R. T1 - Phosphorylation of the chromatin remodeling factor DPF3a induces cardiac hypertrophy through releasing HEY repressors from DNA JF - Nucleic acids research N2 - DPF3 (BAF45c) is a member of the BAF chromatin remodeling complex. Two isoforms have been described, namely DPF3a and DPF3b. The latter binds to acetylated and methylated lysine residues of histones. Here, we elaborate on the role of DPF3a and describe a novel pathway of cardiac gene transcription leading to pathological cardiac hypertrophy. Upon hypertrophic stimuli, casein kinase 2 phosphorylates DPF3a at serine 348. This initiates the interaction of DPF3a with the transcriptional repressors HEY, followed by the release of HEY from the DNA. Moreover, BRG1 is bound by DPF3a, and is thus recruited to HEY genomic targets upon interaction of the two components. Consequently, the transcription of downstream targets such as NPPA and GATA4 is initiated and pathological cardiac hypertrophy is established. In human, DPF3a is significantly up-regulated in hypertrophic hearts of patients with hypertrophic cardiomyopathy or aortic stenosis. Taken together, we show that activation of DPF3a upon hypertrophic stimuli switches cardiac fetal gene expression from being silenced by HEY to being activated by BRG1. Thus, we present a novel pathway for pathological cardiac hypertrophy, whose inhibition is a long-term therapeutic goal for the treatment of the course of heart failure. Y1 - 2016 U6 - https://doi.org/10.1093/nar/gkv1244 SN - 0305-1048 SN - 1362-4962 VL - 44 SP - 2538 EP - 2553 PB - Oxford Univ. Press CY - Oxford ER - TY - JOUR A1 - de Vinuesa, Amaya Garcia A1 - Abdelilah-Seyfried, Salim A1 - Knaus, Petra A1 - Zwijsen, An A1 - Bailly, Sabine T1 - BMP signaling in vascular biology and dysfunction JF - New journal of physics : the open-access journal for physics N2 - The vascular system is critical for developmental growth, tissue homeostasis and repair but also for tumor development. Bone morphogenetic protein (BMP) signaling has recently emerged as a fundamental pathway of the endothelium by regulating cardiovascular and lymphatic development and by being causative for several vascular dysfunctions. Two vascular disorders have been directly linked to impaired BMP signaling: pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia. Endothelial BMP signaling critically depends on the cellular context, which includes among others vascular heterogeneity, exposure to flow, and the intertwining with other signaling cascades (Notch, WNT, Hippo and hypoxia). The purpose of this review is to highlight the most recent findings illustrating the clear need for reconsidering the role of BMPs in vascular biology. (C) 2015 Elsevier Ltd. All rights reserved. KW - Bone morphogenetic proteins (BMP) KW - Signaling KW - Vasculature KW - Development KW - Disease Y1 - 2016 U6 - https://doi.org/10.1016/j.cytogfr.2015.12.005 SN - 1359-6101 SN - 1879-0305 VL - 27 SP - 65 EP - 79 PB - Elsevier CY - Oxford ER -