Götz, Alexander A.

[["dc.bibliographiccitation.firstpage","1083"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1099"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","John, Michael"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Borisch, Angela"],["dc.contributor.author","Boutin, Philippe"],["dc.contributor.author","Neumann, Konstantin"],["dc.contributor.author","Bremes, Vanessa"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Waetzig, Vicky"],["dc.contributor.author","Herdegen, Thomas"],["dc.contributor.author","Teismann, Peter"],["dc.contributor.author","Greig, Iain"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Rotshenker, Shlomo"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:56:53Z"],["dc.date.available","2018-11-07T09:56:53Z"],["dc.date.issued","2015"],["dc.description.abstract","The putative protein tyrosine kinase (PTK) inhibitor tyrphostin AG126 has proven beneficial in various models of inflammatory disease. Yet molecular targets and cellular mechanisms remained enigmatic. We demonstrate here that AG126 treatment has beneficial effects in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. AG126 alleviates the clinical symptoms, diminishes encephalitogenic Th17 differentiation, reduces inflammatory CNS infiltration as well as microglia activation and attenuates myelin damage. We show that AG126 directly inhibits Bruton's tyrosine kinase (BTK), a PTK associated with B cell receptor and Toll-like receptor (TLR) signaling. However, BTK inhibition cannot account for the entire activity spectrum. Effects on TLR-induced proinflammatory cytokine expression in microglia involve AG126 hydrolysis and conversion of its dinitrile side chain to malononitrile (MN). Notably, while liberated MN can subsequently mediate critical AG126 features, full protection in EAE still requires delivery of intact AG126. Its anti-inflammatory potential and especially interference with TLR signaling thus rely on a dual mechanism encompassing BTK and a novel MN-sensitive target. Both principles bear great potential for the therapeutic management of disturbed innate and adaptive immune functions. GLIA 2015;63:1083-1099"],["dc.identifier.doi","10.1002/glia.22803"],["dc.identifier.isi","000353244400011"],["dc.identifier.pmid","25731696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37056"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Tyrphostin AG126 Exerts Neuroprotection in CNS Inflammation by a Dual Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Nau, R."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hanisch, U-K"],["dc.date.accessioned","2018-11-07T09:23:23Z"],["dc.date.available","2018-11-07T09:23:23Z"],["dc.date.issued","2013"],["dc.format.extent","S181"],["dc.identifier.isi","000320408400581"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29563"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","11th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","0894-1491"],["dc.title","CD14 AS A KEY REGULATOR OF TLR-MEDIATED RESPONSES OF MICROGLIA"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","95"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Barrantes-freer, Alonso"],["dc.contributor.author","Mortensen, Lena Sünke"],["dc.contributor.author","Lohrberg, Melanie"],["dc.contributor.author","Götz, Alexander"],["dc.contributor.author","Hanisch, Uwe-karsten"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.date.accessioned","2022-03-01T11:45:14Z"],["dc.date.available","2022-03-01T11:45:14Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.255"],["dc.identifier.pii","S0165572814004883"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103259"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0165-5728"],["dc.title","MyD88 signaling mediates the effects of the innate immune response in cerebellar short-term synaptic plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","217"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","232"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Günther, R."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Jansen, J."],["dc.contributor.author","Balck, A."],["dc.contributor.author","Saal, K.-A."],["dc.contributor.author","Barski, E."],["dc.contributor.author","Nientied, T."],["dc.contributor.author","Götz, A. A."],["dc.contributor.author","Koch, J.-C."],["dc.contributor.author","Mueller, B. K."],["dc.contributor.author","Weishaupt, J. H."],["dc.contributor.author","Sereda, M. W."],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Disease progression in amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motoneurons (MN) and their axons, but is also influenced by neighboring cells such as astrocytes and microglial cells. The role of microglia in ALS is complex as it switches from an anti-inflammatory and neuroprotective phenotype in early disease to a proinflammatory and neurotoxic phenotype in later stages. Our previous studies in models of neurodegeneration identified rho kinase (ROCK) as a target, which can be manipulated to beneficially influence disease progression. Here, we examined the neuroprotective potential of the ROCK inhibitor Fasudil to target the central pathogenic features of ALS. Application of Fasudil to kainic acid-lesioned primary MN in vitro resulted in a strong prosurvival effect. In vivo, SOD1(G93A) mice benefited from oral treatment with Fasudil showing prolonged survival and improved motor function. These findings were correlated to an improved survival of motor neurons and a pronounced alteration of astroglial and microglial cell infiltration of the spinal cord under Fasudil treatment. Modeling a proinflammatory microglial phenotype by stimulation with LPS in vitro, Fasudil decreased the release of proinflammatory cytokines and chemokines TNF, Il6, CCL2, CCL3, and CCL5 while CXCL1 release was only transiently suppressed. In sciatic nerve motor axons, neuromuscular junction remodeling processes were increased. In conclusion, we provide preclinical and neurobiological evidence that inhibition of ROCK by the clinically approved small molecule inhibitor Fasudil may be a novel therapeutic approach in ALS combining both neuroprotection and immunomodulation for the cure of this devastating disease. GLIA 2014;62:217-232"],["dc.identifier.doi","10.1002/glia.22601"],["dc.identifier.gro","3142195"],["dc.identifier.isi","000328209300005"],["dc.identifier.pmid","24311453"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5588"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Rho Kinase Inhibition Modulates Microglia Activation and Improves Survival in a Model of Amyotrophic Lateral Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["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","635"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","649"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Böttcher, Chotima"],["dc.contributor.author","Holtman, Inge R."],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Rossum, Denise van"],["dc.contributor.author","Götz, Alexander"],["dc.contributor.author","Ernst, Anne-Sophie"],["dc.contributor.author","Fritsche, Christin"],["dc.contributor.author","Gertig, Ulla"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Gronke, Konrad"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Rolfes, Simone"],["dc.contributor.author","Weinstein, Jonathan"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Kopatz, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Eggen, Bart J. L."],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2017-09-07T11:45:34Z"],["dc.date.available","2017-09-07T11:45:34Z"],["dc.date.issued","2016"],["dc.description.abstract","Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon β-mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced CNS responses to bacterial infection, traumatic and ischemic injuries, since CD14 deficiency causes either hypo- or hyperinflammation, insufficient or exaggerated immune cell recruitment or worsened stroke outcomes. While CD14 orchestrates functions of TLR4 and related immune receptors, it is itself regulated by TLR and non-TLR systems to thereby fine-tune microglial damage-sensing capacity upon infectious and non-infectious CNS challenges."],["dc.identifier.doi","10.1002/glia.22955"],["dc.identifier.gro","3150405"],["dc.identifier.pmid","26683584"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7166"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0894-1491"],["dc.title","CD14 is a key organizer of microglial responses to CNS infection and injury"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["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"]]