Schumacher, Johannes

[["dc.bibliographiccitation.firstpage","14175"],["dc.bibliographiccitation.issue","49"],["dc.bibliographiccitation.journal","Langmuir : the ACS journal of surfaces and colloids"],["dc.bibliographiccitation.lastpage","14183"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Teske, Nelli"],["dc.contributor.author","Sibold, Jeremias"],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Teiwes, Nikolas K."],["dc.contributor.author","Gleisner, Martin"],["dc.contributor.author","Mey, Ingo"],["dc.contributor.author","Steinem, Claudia"],["dc.date.accessioned","2018-01-17T13:00:51Z"],["dc.date.available","2018-01-17T13:00:51Z"],["dc.date.issued","2017"],["dc.description.abstract","A number of techniques has been developed and analyzed in recent years to generate pore-spanning membranes (PSMs). While quite a number of methods rely on nanoporous substrates, only a few use micrometer-sized pores to be able to individually resolve suspending membranes by means of fluorescence microscopy. To be able to produce PSMs on pores that are micrometer in size, an orthogonal functionalization strategy resulting in a hydrophilic surface is highly desirable. Here, we report on a method to prepare PSMs based on the evaporation of a thin layer of silicon monoxide on top of the porous substrate. PM-IRRAS experiments demonstrate that the final surface is composed of SiOx with 1 < x < 2. The hydrophilic surface turned out to be well suited to spread giant unilamellar vesicles forming PSMs. As the method does not rely on a gold coating as frequently used for orthogonal functionalization, fluorescence micrographs provide information not only from the freestanding membrane areas but also from the supported ones. The observation of the entire PSM area enabled us to observe phase-separation in these membranes on the freestanding and supported parts as well as protein binding and possible lipid reorganization of the membranes induced by binding of the protein Shiga toxin."],["dc.identifier.doi","10.1021/acs.langmuir.7b02727"],["dc.identifier.pmid","29148811"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11698"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1520-5827"],["dc.title","Continuous Pore-Spanning Lipid Bilayers on Silicon Oxide-Coated Porous Substrates"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1425"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics Part B Neuropsychiatric Genetics"],["dc.bibliographiccitation.lastpage","1433"],["dc.bibliographiccitation.volume","153B"],["dc.contributor.author","Mathieu, Flavie"],["dc.contributor.author","Dizier, Marie-Helene"],["dc.contributor.author","Etain, Bruno"],["dc.contributor.author","Jamain, Stephane"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Albus, Margot"],["dc.contributor.author","McKeon, Patrick"],["dc.contributor.author","Roche, Siobhan"],["dc.contributor.author","Blackwood, Douglas"],["dc.contributor.author","Muir, Walter J."],["dc.contributor.author","Henry, Chantal"],["dc.contributor.author","Malafosse, Alain"],["dc.contributor.author","Preisig, Martin"],["dc.contributor.author","Ferrero, Francois"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Ohlraun, Stephanie"],["dc.contributor.author","Propping, Peter"],["dc.contributor.author","Abou Jamra, Rami"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Zelenica, Diana"],["dc.contributor.author","Charon, Celine"],["dc.contributor.author","Marusic, Andrej"],["dc.contributor.author","Dernovsek, Mojca C."],["dc.contributor.author","Gurling, Hugh"],["dc.contributor.author","Noethen, Markus"],["dc.contributor.author","Lathrop, Mark"],["dc.contributor.author","Leboyer, Marion"],["dc.contributor.author","Bellivier, Frank"],["dc.date.accessioned","2018-11-07T08:35:56Z"],["dc.date.available","2018-11-07T08:35:56Z"],["dc.date.issued","2010"],["dc.description.abstract","Bipolar disorder has a genetic component, but the mode of inheritance remains unclear. A previous genome scan conducted in 70 European families led to detect eight regions linked to bipolar disease. Here, we present an investigation of whether the phenotypic heterogeneity of the disorder corresponds to genetic heterogeneity in these regions using additional markers and an extended sample of families. The MLS statistic was used for linkage analyses. The predivided sample test and the maximum likelihood binomial methods were used to test genetic homogeneity between early-onset bipolar type I (cut-off of 22 years) and other types of the disorder (later onset of bipolar type I and early-onset bipolar type II), using a total of 138 independent bipolar-affected sib-pairs. Analysis of the extended sample of families supports linkage in four regions (2q14, 3p14, 16p23, and 20p12) of the eight regions of linkage suggested by our previous genome scan. Heterogeneity testing revealed genetic heterogeneity between early and late-onset bipolar type I in the 2q14 region (P=0.0001). Only the early form of the bipolar disorder but not the late form appeared to be linked to this region. This region may therefore include a genetic factor either specifically involved in the early-onset bipolar type I or only influencing the age at onset (AAO). Our findings illustrate that stratification according to AAO may be valuable for the identification of genetic vulnerability polymorphisms. (C) 2010 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/ajmg.b.31121"],["dc.identifier.isi","000284623200006"],["dc.identifier.pmid","20886542"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18198"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1552-4841"],["dc.title","European Collaborative Study of Early-Onset Bipolar Disorder: Evidence for Genetic Heterogeneity on 2q14 According to Age at Onset"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","8450"],["dc.bibliographiccitation.journal","J. Mater. Chem. A"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Assaud, Loïc"],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Tafel, Alexander"],["dc.contributor.author","Bochmann, Sebastian"],["dc.contributor.author","Christiansen, Silke"],["dc.contributor.author","Bachmann, Julien"],["dc.date.accessioned","2015-12-09T11:01:30Z"],["dc.date.accessioned","2021-10-27T13:12:24Z"],["dc.date.available","2015-12-09T11:01:30Z"],["dc.date.available","2021-10-27T13:12:24Z"],["dc.date.issued","2015"],["dc.description.abstract","We establish a procedure for the fabrication of electrocatalytically active, nanoporous surfaces coated with Pt and exhibiting a high geometric area. Firstly, the mechanism of the surface reactions between platinum(II) acetylacetonate and ozone is investigated by piezoelectric microbalance measurements. The data reveal that ozone oxidizes the metallic Pt surface to an extent which can exceed one monolayer depending on the reaction conditions. Proper reaction parameters yield a self-limited growth in atomic layer deposition (ALD) mode. Secondly, the ALD procedure is applied to porous anodic oxide substrates. The morphology and the crystal structure of the deposits are characterized. The ALD coating results in a continuous layer of Pt nanocrystallites along deep pore walls (aspect ratio 70). Thirdly, the Pt/TiO2 surfaces are shown to be electrochemically active in both acidic and alkaline media, in a way that qualitatively conforms to literature precedents based on Pt. Finally, we apply the anodization and ALD procedure to commercial Ti felts and demonstrate systematically how the electrochemical current density is increased by the large specific surface area and by the presence of the catalyst. Thereby, the catalyst loading, as well as its efficient utilization, can be optimized accurately. The preparative approach demonstrated here can be generalized and applied to the various electrocatalytic reactions of energy conversion devices."],["dc.identifier.doi","10.1039/C5TA00205B"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12608"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91689"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/312284/EU//CALIPSO"],["dc.relation.euproject","CALIPSO"],["dc.relation.issn","2050-7496"],["dc.relation.issn","2050-7488"],["dc.relation.orgunit","Fakultät für Chemie"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","electrocatalytic turnover; nanoporous platinum surfaces; atomic layer deposition"],["dc.title","Systematic increase of electrocatalytic turnover at nanoporous platinum surfaces prepared by atomic layer deposition"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The American Journal of Human Genetics"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Miro, Xavier"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Steffens, Michael"],["dc.contributor.author","Meesters, Christian"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Weingarten, Moritz"],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Haenisch, Britta"],["dc.contributor.author","Alexander, Michael J."],["dc.contributor.author","Vollmer, Jennifer"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Schmael, Christine"],["dc.contributor.author","Tessmann, Peter"],["dc.contributor.author","Moebus, Susanne"],["dc.contributor.author","Wichmann, Heinz-Erich"],["dc.contributor.author","Schreiber, Stefan"],["dc.contributor.author","Mueller-Myhsok, Bertram"],["dc.contributor.author","Lucae, Susanne"],["dc.contributor.author","Jamain, Stephane"],["dc.contributor.author","Leboyer, Marion"],["dc.contributor.author","Bellivier, Frank"],["dc.contributor.author","Etain, Bruno"],["dc.contributor.author","Henry, Chantal"],["dc.contributor.author","Kahn, Jean-Pierre"],["dc.contributor.author","Heath, Simon"],["dc.contributor.author","Hamshere, Marian L."],["dc.contributor.author","O'Donovan, Michael C."],["dc.contributor.author","Owen, Michael J."],["dc.contributor.author","Craddock, Nick"],["dc.contributor.author","Schwarz, Markus"],["dc.contributor.author","Vedder, Helmut"],["dc.contributor.author","Kammerer-Ciernioch, Jutta"],["dc.contributor.author","Reif, Andreas"],["dc.contributor.author","Sasse, Johanna"],["dc.contributor.author","Bauer, Michael"],["dc.contributor.author","Hautzinger, Martin"],["dc.contributor.author","Wright, Adam"],["dc.contributor.author","Mitchell, Philip B."],["dc.contributor.author","Schofield, Peter R."],["dc.contributor.author","Montgomery, Grant W."],["dc.contributor.author","Medland, Sarah E."],["dc.contributor.author","Gordon, Scott D."],["dc.contributor.author","Martin, Nicholas G."],["dc.contributor.author","Gustafsson, Omar"],["dc.contributor.author","Andreassen, Ole A."],["dc.contributor.author","Djurovic, Srdjan"],["dc.contributor.author","Sigurdsson, Engilbert"],["dc.contributor.author","Steinberg, Stacy"],["dc.contributor.author","Stefansson, Hreinn"],["dc.contributor.author","Stefansson, Kari"],["dc.contributor.author","Kapur-Pojskic, Lejla"],["dc.contributor.author","Oruc, Liliana"],["dc.contributor.author","Rivas, Fabio"],["dc.contributor.author","Mayoral, Fermin"],["dc.contributor.author","Chuchalin, Alexander"],["dc.contributor.author","Babadjanova, Gulja"],["dc.contributor.author","Tiganov, Alexander S."],["dc.contributor.author","Pantelejeva, Galina"],["dc.contributor.author","Abramova, Lilia I."],["dc.contributor.author","Grigoroiu-Serbanescu, Maria"],["dc.contributor.author","Diaconu, Carmen C."],["dc.contributor.author","Czerski, Piotr M."],["dc.contributor.author","Hauser, Joanna"],["dc.contributor.author","Zimmer, Andreas"],["dc.contributor.author","Lathrop, Mark"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Wienker, Thomas F."],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Propping, Peter"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Noethen, Markus M."],["dc.date.accessioned","2018-11-07T08:58:10Z"],["dc.date.available","2018-11-07T08:58:10Z"],["dc.date.issued","2011"],["dc.format.extent","396"],["dc.identifier.doi","10.1016/j.ajhg.2011.03.001"],["dc.identifier.isi","000288589000019"],["dc.identifier.pmid","21353194"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","0002-9297"],["dc.title","Genome-wide Association Study Identifies Genetic Variation in Neurocan as a Susceptibility Factor for Bipolar Disorder (vol 88, pg 372, 2011)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","24"],["dc.bibliographiccitation.issue","1-3"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","30"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Nieratschker, Vanessa"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Wendland, Jens R."],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Abou Jamra, Rami"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Schmael, Christine"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2018-11-07T08:40:11Z"],["dc.date.available","2018-11-07T08:40:11Z"],["dc.date.issued","2010"],["dc.description.abstract","The aim of the present study was to investigate possible associations between schizophrenia and 13 SNP markers in COMT. No association was observed in 631 cases, 207 nuclear families, and 776 controls. A cognitive performance phenotype (Trail Marking Test) was available for a subgroup of the patients. No association was found between the 13 markers and this phenotype. Four clinically-defined subgroups (early age at onset, negative symptoms, family history of schizophrenia, and life-time major depressive episode) were also investigated. Associations were observed for 3 of these subgroups, although none withstood correction for multiple testing. COMT does not appear to be a risk factor for schizophrenia in this population. (C) 2010 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.schres.2010.06.018"],["dc.identifier.isi","000286406900002"],["dc.identifier.pmid","20643532"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19164"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0920-9964"],["dc.title","The catechol-O-methyl transferase (COMT) gene and its potential association with schizophrenia: Findings from a large German case-control and family-based sample"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","906"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","917"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Kirsch, Peter"],["dc.contributor.author","Esslinger, Christine"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Demontis, D."],["dc.contributor.author","Steffens, Michael"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Haenisch, Britta"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Czerski, Piotr M."],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Strengman, E."],["dc.contributor.author","Schmael, C."],["dc.contributor.author","Mors, Ole"],["dc.contributor.author","Mortensen, Preben Bo"],["dc.contributor.author","Hougaard, D. M."],["dc.contributor.author","Orntoft, Torben F."],["dc.contributor.author","Kapelski, P."],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Basmanav, F. Buket U."],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Hoffmann, P."],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Nikitopoulos, J."],["dc.contributor.author","Moebus, Susanne"],["dc.contributor.author","Alexander, M."],["dc.contributor.author","Moessner, R."],["dc.contributor.author","Wichmann, H-E"],["dc.contributor.author","Schreiber, S."],["dc.contributor.author","Rivandeneira, Fernando"],["dc.contributor.author","Hofman, Albert"],["dc.contributor.author","Uitterlinden, Andre G."],["dc.contributor.author","Wienker, Thomas F."],["dc.contributor.author","Schumacher, J."],["dc.contributor.author","Hauser, Joanna"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Cantor, R. M."],["dc.contributor.author","Erk, S."],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Craddock, N."],["dc.contributor.author","Owen, M. J."],["dc.contributor.author","O'Donovan, M. C."],["dc.contributor.author","Borglum, Anders D."],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Walter, H."],["dc.contributor.author","Meyer-Lindenberg, Andreas"],["dc.contributor.author","Noethen, M. M."],["dc.contributor.author","Ophoff, Roel A."],["dc.contributor.author","Cichon, Sven"],["dc.date.accessioned","2018-11-07T09:06:48Z"],["dc.date.available","2018-11-07T09:06:48Z"],["dc.date.issued","2012"],["dc.description.abstract","Recent molecular studies have implicated common alleles of small to moderate effect and rare alleles with larger effect sizes in the genetic architecture of schizophrenia (SCZ). It is expected that the reliable detection of risk variants with very small effect sizes can only be achieved through the recruitment of very large samples of patients and controls (that is tens of thousands), or large, potentially more homogeneous samples that have been recruited from confined geographical areas using identical diagnostic criteria. Applying the latter strategy, we performed a genome-wide association study (GWAS) of 1169 clinically well characterized and ethnically homogeneous SCZ patients from a confined area of Western Europe (464 from Germany, 705 from The Netherlands) and 3714 ethnically matched controls (1272 and 2442, respectively). In a subsequent follow-up study of our top GWAS results, we included an additional 2569 SCZ patients and 4088 controls (from Germany, The Netherlands and Denmark). Genetic variation in a region on chromosome 11 that contains the candidate genes AMBRA1, DGKZ, CHRM4 and MDK was significantly associated with SCZ in the combined sample (n = 11 540; P = 3.89 x 10(-9), odds ratio (OR) = 1.25). This finding was replicated in 23 206 independent samples of European ancestry (P = 0.0029, OR= 1.11). In a subsequent imaging genetics study, healthy carriers of the risk allele exhibited altered activation in the cingulate cortex during a cognitive control task. The area of interest is a critical interface between emotion regulation and cognition that is structurally and functionally abnormal in SCZ and bipolar disorder. Molecular Psychiatry (2012) 17, 906-917; doi: 10.1038/mp.2011.80; published online 12 July 2011"],["dc.identifier.doi","10.1038/mp.2011.80"],["dc.identifier.isi","000308063900007"],["dc.identifier.pmid","21747397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25636"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1476-5578"],["dc.relation.issn","1359-4184"],["dc.title","Association between genetic variation in a region on chromosome 11 and schizophrenia in large samples from Europe"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","9234"],["dc.bibliographiccitation.issue","27"],["dc.bibliographiccitation.journal","Angewandte Chemie. International Edition"],["dc.bibliographiccitation.lastpage","9238"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Schilling, Nadine A."],["dc.contributor.author","Berscheid, Anne"],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Saur, Julian S."],["dc.contributor.author","Konnerth, Martin C."],["dc.contributor.author","Wirtz, Sebastian N."],["dc.contributor.author","Beltrán‐Beleña, José M."],["dc.contributor.author","Zipperer, Alexander"],["dc.contributor.author","Krismer, Bernhard"],["dc.contributor.author","Grond, Stephanie"],["dc.date.accessioned","2021-06-01T10:49:28Z"],["dc.date.available","2021-06-01T10:49:28Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/anie.201901589"],["dc.identifier.eissn","1521-3773"],["dc.identifier.issn","1433-7851"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16711"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86304"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1521-3773"],["dc.relation.issn","1433-7851"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Synthetic Lugdunin Analogues Reveal Essential Structural Motifs for Antimicrobial Action and Proton Translocation Capability"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2670"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","The Analyst"],["dc.bibliographiccitation.lastpage","2677"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Schwamborn, Miriam"],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Sibold, Jeremias"],["dc.contributor.author","Teiwes, Nikolas K."],["dc.contributor.author","Steinem, Claudia"],["dc.date.accessioned","2018-01-17T13:03:01Z"],["dc.date.available","2018-01-17T13:03:01Z"],["dc.date.issued","2017"],["dc.description.abstract","Monitoring the proton pumping activity of proteins such as ATPases in reconstituted single proteoliposomes is key to quantify the function of proteins as well as potential proton pump inhibitors. However, most pH-detecting assays available are either not quantitative, require well-adapted reconstitution protocols or are not appropriate for single vesicle studies. Here, we describe the quantitative and time-resolved detection of F-type ATPase-induced pH changes across vesicular membranes doped with the commercially available pH sensitive fluorophore Oregon Green 488 DHPE. This dye is shown to be well suited to monitor acidification of lipid vesicles not only in bulk but also at the single vesicle level. The pKa value of Oregon Green 488 DHPE embedded in a lipid environment was determined to be 6.1 making the fluorophore well suited for a variety of physiologically relevant proton pumps. The TFOF1-ATPase from a thermophilic bacterium was reconstituted into large unilamellar vesicles and the bulk acidification assay clearly reveals the overall activity of the F-type ATPase in the vesicle ensemble with an average pH change of 0.45. However, monitoring the pH changes in individual vesicles attached to a substrate demonstrates that the fraction of vesicles with a significant observable pH change is only about 5%, a number that cannot be gathered from bulk experiments and which is considerably lower than expected."],["dc.identifier.doi","10.1039/c7an00215g"],["dc.identifier.pmid","28616949"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11701"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1364-5528"],["dc.title","Monitoring ATPase induced pH changes in single proteoliposomes with the lipid-coupled fluorophore Oregon Green 488"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","214"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Plant Molecular Biology Reporter"],["dc.bibliographiccitation.lastpage","223"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Vornam, B."],["dc.contributor.author","Leinemann, Ludger"],["dc.contributor.author","Peters, F. S."],["dc.contributor.author","Wolff, A."],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Salinas, G."],["dc.contributor.author","Schumacher, J."],["dc.contributor.author","Gailing, Oliver"],["dc.date.accessioned","2020-05-14T07:37:58Z"],["dc.date.available","2020-05-14T07:37:58Z"],["dc.date.issued","2019"],["dc.description.abstract","The ascomycete Sphaeropsis sapinea (syn. Diplodia pinea), the causal agent of Diplodia blight of pine, is also known to be an endophyte with a latent pathogenic potential on pine trees. Due to climate change effects, especially warming and more prolonged or frequent drought events, the hosts are weakened and S. sapinea could become more aggressive in the future. Normally, pines which are 25 years old or older are more susceptible to the disease as compared with younger trees. However, if younger trees are growing on poor sites or are located close to affected trees, they may also become infected. Here, we analyzed the interaction of young pine seedlings (4 years old) with the fungus in vitro, in order to examine the changes in gene activity for example of genes encoding metabolites and therewith contributing to an induced resistance against the fungus. During different stages of infection (control without infection and 14 days after infection), pine needles of four samples per stage (eight samples all together) were collected and analyzed by mRNA sequencing. The comparison between the two stages showed that, nearly independent of the genotype of the plant, 5691 genes were differentially expressed. In the severe stage of infection, elevated transcript levels of genes involved in lignin- and phytoalexin-biosynthesis and of pathogenesis-related genes were found. Furthermore, some of these genes were also validated in a natural population of Pinus sylvestris by reverse transcriptase (RT)-PCR in order to analyze induced defense responses."],["dc.identifier.doi","10.1007/s11105-019-01149-2"],["dc.identifier.scopus","2-s2.0-85065250893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/65405"],["dc.identifier.url","http://www.scopus.com/inward/record.url?eid=2-s2.0-85065250893&partnerID=MN8TOARS"],["dc.language.iso","en"],["dc.relation.eissn","1572-9818"],["dc.relation.issn","0735-9640"],["dc.title","Response of Scots pine (Pinus sylvestris) seedlings subjected to artificial infection with the fungus Sphaeropsis sapinea"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","3339"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Leber, Markus"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Hoffmann, Per"],["dc.contributor.author","Lacour, Andre"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Reif, Andreas"],["dc.contributor.author","Müller-Myhsok, Bertram"],["dc.contributor.author","Lucae, Susanne"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Schwarz, Markus"],["dc.contributor.author","Vedder, Helmut"],["dc.contributor.author","Kammerer-Ciernioch, Jutta"],["dc.contributor.author","Pfennig, Andrea"],["dc.contributor.author","Bauer, Michael"],["dc.contributor.author","Hautzinger, Martin"],["dc.contributor.author","Moebus, Susanne"],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Czerski, Piotr M."],["dc.contributor.author","Hauser, Joanna"],["dc.contributor.author","Lissowska, Jolanta"],["dc.contributor.author","Szeszenia-Dabrowska, Neonila"],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","McKay, James D."],["dc.contributor.author","Wright, Adam"],["dc.contributor.author","Mitchell, Philip B."],["dc.contributor.author","Fullerton, Janice M."],["dc.contributor.author","Schofield, Peter R."],["dc.contributor.author","Montgomery, Grant W."],["dc.contributor.author","Medland, Sarah E."],["dc.contributor.author","Gordon, Scott D."],["dc.contributor.author","Martin, Nicholas G."],["dc.contributor.author","Krasnow, Valery"],["dc.contributor.author","Chuchalin, Alexander"],["dc.contributor.author","Babadjanova, Gulja"],["dc.contributor.author","Pantelejeva, Galina"],["dc.contributor.author","Abramova, Lilia I."],["dc.contributor.author","Tiganov, Alexander S."],["dc.contributor.author","Polonikov, Alexey"],["dc.contributor.author","Khusnutdinova, Elza"],["dc.contributor.author","Alda, Martin"],["dc.contributor.author","Grof, Paul"],["dc.contributor.author","Rouleau, Guy A."],["dc.contributor.author","Turecki, Gustavo"],["dc.contributor.author","Laprise, Catherine"],["dc.contributor.author","Rivas, Fabio"],["dc.contributor.author","Mayoral, Fermin"],["dc.contributor.author","Kogevinas, Manolis"],["dc.contributor.author","Grigoroiu-Serbanescu, Maria"],["dc.contributor.author","Propping, Peter"],["dc.contributor.author","Becker, Tim"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Cichon, Sven"],["dc.date.accessioned","2018-11-07T09:42:56Z"],["dc.date.available","2018-11-07T09:42:56Z"],["dc.date.issued","2014"],["dc.description.abstract","Bipolar disorder (BD) is a common and highly heritable mental illness and genome-wide association studies (GWAS) have robustly identified the first common genetic variants involved in disease aetiology. The data also provide strong evidence for the presence of multiple additional risk loci, each contributing a relatively small effect to BD susceptibility. Large samples are necessary to detect these risk loci. Here we present results from the largest BD GWAS to date by investigating 2.3 million single-nucleotide polymorphisms (SNPs) in a sample of 24,025 patients and controls. We detect 56 genome-wide significant SNPs in five chromosomal regions including previously reported risk loci ANK3, ODZ4 and TRANK1, as well as the risk locus ADCY2 (5p15.31) and a region between MIR2113 and POU3F2 (6q16.1). ADCY2 is a key enzyme in cAMP signalling and our finding provides new insights into the biological mechanisms involved in the development of BD."],["dc.identifier.doi","10.1038/ncomms4339"],["dc.identifier.isi","000334295200001"],["dc.identifier.pmid","24618891"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34073"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","2041-1723"],["dc.title","Genome-wide association study reveals two new risk loci for bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]