Götz, Alexander A.

[["dc.bibliographiccitation.firstpage","18614"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Journal of Biological Chemistry"],["dc.bibliographiccitation.lastpage","18622"],["dc.bibliographiccitation.volume","286"],["dc.contributor.author","Horsch, Marion"],["dc.contributor.author","Seeburg, Peter H."],["dc.contributor.author","Adler, Thure"],["dc.contributor.author","Aguilar-Pimentel, Juan Antonio"],["dc.contributor.author","Becker, Lore"],["dc.contributor.author","Calzada-Wack, Julia"],["dc.contributor.author","Garrett, Lilian"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Hans, Wolfgang"],["dc.contributor.author","Higuchi, Miyoko"],["dc.contributor.author","Hoelter, Sabine M."],["dc.contributor.author","Naton, Beatrix"],["dc.contributor.author","Prehn, Cornelia"],["dc.contributor.author","Puk, Oliver"],["dc.contributor.author","Racz, Ildiko"],["dc.contributor.author","Rathkolb, Birgit"],["dc.contributor.author","Rozman, Jan"],["dc.contributor.author","Schrewe, Anja"],["dc.contributor.author","Adamski, Jerzy"],["dc.contributor.author","Busch, Dirk H."],["dc.contributor.author","Esposito, Irene"],["dc.contributor.author","Graw, Jochen"],["dc.contributor.author","Ivandic, Boris"],["dc.contributor.author","Klingenspor, Martin"],["dc.contributor.author","Klopstock, Thomas"],["dc.contributor.author","Mempel, Martin"],["dc.contributor.author","Ollert, Markus W."],["dc.contributor.author","Schulz, Holger"],["dc.contributor.author","Wolf, Eckhard"],["dc.contributor.author","Wurst, Wolfgang"],["dc.contributor.author","Zimmer, Andreas"],["dc.contributor.author","Gailus-Durner, Valerie"],["dc.contributor.author","Fuchs, Helmut"],["dc.contributor.author","de Angelis, Martin Hrabe"],["dc.contributor.author","Beckers, Johannes"],["dc.date.accessioned","2018-11-07T08:56:01Z"],["dc.date.available","2018-11-07T08:56:01Z"],["dc.date.issued","2011"],["dc.description.abstract","ADAR2, an RNA editing enzyme that converts specific adenosines to inosines in certain pre-mRNAs, often leading to amino acid substitutions in the encoded proteins, is mainly expressed in brain. Of all ADAR2-mediated edits, a single one in the pre-mRNA of the AMPA receptor subunit GluA2 is essential for survival. Hence, early postnatal death of mice lacking ADAR2 is averted when the critical edit is engineered into both GluA2 encoding Gria2 alleles. Adar2(-/-)/Gria2(R/R) mice display normal appearance and life span, but the general phenotypic effects of global lack of ADAR2 have remained unexplored. Here we have employed the Adar2(-/-)/Gria2(R/R) mouse line, and Gria2(R/R) mice as controls, to study the phenotypic consequences of loss of all ADAR2-mediated edits except the critical one in GluA2. Our extended phenotypic analysis covering similar to 320 parameters identified significant changes related to absence of ADAR2 in behavior, hearing ability, allergy parameters and transcript profiles of brain."],["dc.identifier.doi","10.1074/jbc.M110.200881"],["dc.identifier.isi","000290785700033"],["dc.identifier.pmid","21467037"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23045"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Biochemistry Molecular Biology Inc"],["dc.relation.issn","0021-9258"],["dc.title","Requirement of the RNA-editing Enzyme ADAR2 for Normal Physiology in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","L1114"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","AJP Lung Cellular and Molecular Physiology"],["dc.bibliographiccitation.lastpage","L1124"],["dc.bibliographiccitation.volume","308"],["dc.contributor.author","Holm, Anne Trommelholt"],["dc.contributor.author","Wulf-Johansson, Helle"],["dc.contributor.author","Hvidsten, Svend"],["dc.contributor.author","Jorgensen, Patricia Troest"],["dc.contributor.author","Schlosser, Anders"],["dc.contributor.author","Pilecki, Bartosz"],["dc.contributor.author","Ormhoj, Maria"],["dc.contributor.author","Moeller, Jesper Bonnet"],["dc.contributor.author","Johannsen, Claus"],["dc.contributor.author","Baun, Christina"],["dc.contributor.author","Andersen, Thomas"],["dc.contributor.author","Schneider, Jan Philipp"],["dc.contributor.author","Hegermann, Jan"],["dc.contributor.author","Ochs, Matthias"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Schulz, Holger"],["dc.contributor.author","de Angelis, Martin Hrabe"],["dc.contributor.author","Vestbo, Jorgen"],["dc.contributor.author","Holmskov, Uffe"],["dc.contributor.author","Sorensen, Grith Lykke"],["dc.date.accessioned","2018-11-07T09:56:18Z"],["dc.date.available","2018-11-07T09:56:18Z"],["dc.date.issued","2015"],["dc.description.abstract","Microfibrillar-associated protein 4 (MFAP4) is localized to elastic fibers in blood vessels and the interalveolar septa of the lungs and is further present in bronchoalveolar lavage. Mfap4 has been previously suggested to be involved in elastogenesis in the lung. We tested this prediction and aimed to characterize the pulmonary function changes and emphysematous changes that occur in Mfap4-deficient (Mfap4(-/-)) mice. Significant changes included increases in total lung capacity and compliance, which were evident in Mfap4(-/-) mice at 6 and 8 mo but not at 3 mo of age. Using in vivo breath-hold gated microcomputed tomography (micro-CT) in 8-mo-old Mfap4(-/-) mice, we found that the mean density of the lung parenchyma was decreased, and the low-attenuation area (LAA) was significantly increased by 14% compared with Mfap4(+/+) mice. Transmission electron microscopy (TEM) did not reveal differences in the organization of elastic fibers, and there was no difference in elastin content, but a borderline significant increase in elastin mRNA expression in 3-mo-old mice. Stereological analysis showed that alveolar surface density in relation to the lung parenchyma and total alveolar surface area inside of the lung were both significantly decreased in Mfap4(-/-) mice by 25 and 15%, respectively. The data did not support an essential role of MFAP4 in pulmonary elastic fiber organization or content but indicated increased turnover in young Mfap4(-/-) mice. However, Mfap4(-/-) mice developed a spontaneous loss of lung function, which was evident at 6 mo of age, and moderate air space enlargement, with emphysema-like changes."],["dc.identifier.doi","10.1152/ajplung.00351.2014"],["dc.identifier.isi","000357509200003"],["dc.identifier.pmid","26033354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36929"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","1522-1504"],["dc.relation.issn","1040-0605"],["dc.title","Characterization of spontaneous air space enlargement in mice lacking microfibrillar-associated protein 4"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","120"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Methods"],["dc.bibliographiccitation.lastpage","135"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Fuchs, Helmut"],["dc.contributor.author","Gailus-Durner, Valerie"],["dc.contributor.author","Adler, Thure"],["dc.contributor.author","Aguilar-Pimentel, Juan Antonio"],["dc.contributor.author","Becker, Lore"],["dc.contributor.author","Calzada-Wack, Julia"],["dc.contributor.author","Da Silva-Buttkus, Patricia"],["dc.contributor.author","Neff, Frauke"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Hans, Wolfgang"],["dc.contributor.author","Hoelter, Sabine M."],["dc.contributor.author","Horsch, Marion"],["dc.contributor.author","Kastenmueller, Gabi"],["dc.contributor.author","Kemter, Elisabeth"],["dc.contributor.author","Lengger, Christoph"],["dc.contributor.author","Maier, Holger"],["dc.contributor.author","Matloka, Mikolaj"],["dc.contributor.author","Moeller, Gabriele"],["dc.contributor.author","Naton, Beatrix"],["dc.contributor.author","Prehn, Cornelia"],["dc.contributor.author","Puk, Oliver"],["dc.contributor.author","Racz, Ildiko"],["dc.contributor.author","Rathkolb, Birgit"],["dc.contributor.author","Roemisch-Margl, Werner"],["dc.contributor.author","Rozman, Jan"],["dc.contributor.author","Wang-Sattler, Rui"],["dc.contributor.author","Schrewe, Anja"],["dc.contributor.author","Stoeger, Claudia"],["dc.contributor.author","Tost, Monica"],["dc.contributor.author","Adamski, Jerzy"],["dc.contributor.author","Aigner, Bernhard"],["dc.contributor.author","Beckers, Johannes"],["dc.contributor.author","Behrendt, Heidrun"],["dc.contributor.author","Busch, Dirk H."],["dc.contributor.author","Esposito, Irene"],["dc.contributor.author","Graw, Jochen"],["dc.contributor.author","Illig, Thomas"],["dc.contributor.author","Ivandic, Boris"],["dc.contributor.author","Klingenspor, Martin"],["dc.contributor.author","Klopstock, Thomas"],["dc.contributor.author","Kremmer, Elisabeth"],["dc.contributor.author","Mempel, Martin"],["dc.contributor.author","Neschen, Susanne"],["dc.contributor.author","Ollert, Markus W."],["dc.contributor.author","Schulz, Holger"],["dc.contributor.author","Suhre, Karsten"],["dc.contributor.author","Wolf, Eckhard"],["dc.contributor.author","Wurst, Wolfgang"],["dc.contributor.author","Zimmer, Andreas"],["dc.contributor.author","de Angelis, Martin Hrabe"],["dc.date.accessioned","2018-11-07T08:59:53Z"],["dc.date.available","2018-11-07T08:59:53Z"],["dc.date.issued","2011"],["dc.description.abstract","Model organisms like the mouse are important tools to learn more about gene function in man. Within the last 20 years many mutant mouse lines have been generated by different methods such as ENU mutagenesis, constitutive and conditional knock-out approaches, knock-down, introduction of human genes, and knock-in techniques, thus creating models which mimic human conditions. Due to pleiotropic effects, one gene may have different functions in different organ systems or time points during development. Therefore mutant mouse lines have to be phenotyped comprehensively in a highly standardized manner to enable the detection of phenotypes which might otherwise remain hidden. The German Mouse Clinic (GMC) has been established at the Helmholtz Zentrum Munchen as a phenotyping platform with open access to the scientific community (www.mousclinic.de; [1]). The GMC is a member of the EUMOD-IC consortium which created the European standard workflow EMPReSSslim for the systemic phenotyping of mouse models (http://www.eumodic.org/ [2]). (C) 2010 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.ymeth.2010.08.006"],["dc.identifier.isi","000287275900003"],["dc.identifier.pmid","20708688"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24012"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1046-2023"],["dc.title","Mouse phenotyping"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]