Now showing 1 - 10 of 17
  • 2017Journal Article
    [["dc.bibliographiccitation.artnumber","959"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Molecular systems biology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Hatje, Klas"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Simm, Dominic"],["dc.contributor.author","Hammesfahr, Björn"],["dc.contributor.author","Bansal, Vikas"],["dc.contributor.author","Rajput, Ashish"],["dc.contributor.author","Mickael, Michel Edwar"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Kollmar, Martin"],["dc.date.accessioned","2019-07-30T10:25:25Z"],["dc.date.available","2019-07-30T10:25:25Z"],["dc.date.issued","2017"],["dc.description.abstract","Mutually exclusive splicing of exons is a mechanism of functional gene and protein diversification with pivotal roles in organismal development and diseases such as Timothy syndrome, cardiomyopathy and cancer in humans. In order to obtain a first genomewide estimate of the extent and biological role of mutually exclusive splicing in humans, we predicted and subsequently validated mutually exclusive exons (MXEs) using 515 publically available RNA-Seq datasets. Here, we provide evidence for the expression of over 855 MXEs, 42% of which represent novel exons, increasing the annotated human mutually exclusive exome more than fivefold. The data provide strong evidence for the existence of large and multi-cluster MXEs in higher vertebrates and offer new insights into MXE evolution. More than 82% of the MXE clusters are conserved in mammals, and five clusters have homologous clusters in Drosophila Finally, MXEs are significantly enriched in pathogenic mutations and their spatio-temporal expression might predict human disease pathology."],["dc.identifier.doi","10.15252/msb.20177728"],["dc.identifier.pmid","29242366"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62194"],["dc.language.iso","en"],["dc.relation.eissn","1744-4292"],["dc.relation.issn","1744-4292"],["dc.relation.issn","1744-4292"],["dc.relation.issn","1744-4292"],["dc.title","The landscape of human mutually exclusive splicing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2016Journal Article
    [["dc.bibliographiccitation.artnumber","160090"],["dc.bibliographiccitation.journal","Scientific Data"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Bonn, Stefan"],["dc.date.accessioned","2017-09-07T11:52:23Z"],["dc.date.available","2017-09-07T11:52:23Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1038/sdata.2016.90"],["dc.identifier.gro","3144912"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14127"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2588"],["dc.notes.intern","Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","public"],["dc.relation.issn","2052-4463"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Genome-wide chromatin and gene expression profiling during memory formation and maintenance in adult mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2017Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","9"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Fomin, Andrey"],["dc.contributor.author","Luo, Xiaojing"],["dc.contributor.author","Li, Wener"],["dc.contributor.author","Fischer, Claudia"],["dc.contributor.author","Özcelik, Cemil"],["dc.contributor.author","Perrot, Andreas"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Vidal, Ramon Oliveira"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2018-04-23T11:49:17Z"],["dc.date.available","2018-04-23T11:49:17Z"],["dc.date.issued","2017"],["dc.description.abstract","The ability to generate patient-specific induced pluripotent stem cells (iPSCs) provides a unique opportunity for modeling heart disease in vitro. In this study, we generated iPSCs from a patient with dilated cardiomyopathy (DCM) caused by a missense mutation S635A in RNA-binding motif protein 20 (RBM20) and investigated the functionality and cell biology of cardiomyocytes (CMs) derived from patient-specific iPSCs (RBM20-iPSCs). The RBM20-iPSC-CMs showed abnormal distribution of sarcomeric α-actinin and defective calcium handling compared to control-iPSC-CMs, suggesting disorganized myofilament structure and altered calcium machinery in CMs of the RBM20 patient. Engineered heart muscles (EHMs) from RBM20-iPSC-CMs showed that not only active force generation was impaired in RBM20-EHMs but also passive stress of the tissue was decreased, suggesting a higher visco-elasticity of RBM20-EHMs. Furthermore, we observed a reduced titin (TTN) N2B-isoform expression in RBM20-iPSC-CMs by demonstrating a reduction of exon skipping in the PEVK region of TTN and an inhibition of TTN isoform switch. In contrast, in control-iPSC-CMs both TTN isoforms N2B and N2BA were expressed, indicating that the TTN isoform switch occurs already during early cardiogenesis. Using next generation RNA sequencing, we mapped transcriptome and splicing target profiles of RBM20-iPSC-CMs and identified different cardiac gene networks in response to the analyzed RBM20 mutation in cardiac-specific processes. These findings shed the first light on molecular mechanisms of RBM20-dependent pathological cardiac remodeling leading to DCM. Our data demonstrate that iPSC-CMs coupled with EHMs provide a powerful tool for evaluating disease-relevant functional defects and for a deeper mechanistic understanding of alternative splicing-related cardiac diseases."],["dc.identifier.doi","10.1016/j.yjmcc.2017.09.008"],["dc.identifier.gro","3142517"],["dc.identifier.pmid","28941705"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16493"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13672"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/191"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A08: Translationale und posttranslationale Kontrolle trunkierter Titinproteine in Kardiomyozyten von Patienten mit dilatativer Kardiomyopathie"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.issn","0022-2828"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Linke (Kardiovaskuläre Physiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Severe DCM phenotype of patient harboring RBM20 mutation S635A can be modeled by patient-specific induced pluripotent stem cell-derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2018Journal Article Research Paper
    [["dc.bibliographiccitation.artnumber","16913"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Mandad, Sunit"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Wildhagen, Hanna"],["dc.contributor.author","Rammner, Burkhard"],["dc.contributor.author","Keihani, Sarva"],["dc.contributor.author","Opazo, Felipe"],["dc.contributor.author","Urban, Inga"],["dc.contributor.author","Ischebeck, Till"],["dc.contributor.author","Kirli, Koray"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Yousefi, Roya Y."],["dc.contributor.author","Dennerlein, Sven"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Feußner, Ivo"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Fornasiero, Eugenio F."],["dc.date.accessioned","2019-07-09T11:50:21Z"],["dc.date.available","2019-07-09T11:50:21Z"],["dc.date.issued","2018"],["dc.description.abstract","The homeostasis of the proteome depends on the tight regulation of the mRNA and protein abundances, of the translation rates, and of the protein lifetimes. Results from several studies on prokaryotes or eukaryotic cell cultures have suggested that protein homeostasis is connected to, and perhaps regulated by, the protein and the codon sequences. However, this has been little investigated for mammals in vivo. Moreover, the link between the coding sequences and one critical parameter, the protein lifetime, has remained largely unexplored, both in vivo and in vitro. We tested this in the mouse brain, and found that the percentages of amino acids and codons in the sequences could predict all of the homeostasis parameters with a precision approaching experimental measurements. A key predictive element was the wobble nucleotide. G-/C-ending codons correlated with higher protein lifetimes, protein abundances, mRNA abundances and translation rates than A-/U-ending codons. Modifying the proportions of G-/C-ending codons could tune these parameters in cell cultures, in a proof-of-principle experiment. We suggest that the coding sequences are strongly linked to protein homeostasis in vivo, albeit it still remains to be determined whether this relation is causal in nature."],["dc.identifier.doi","10.1038/s41598-018-35277-8"],["dc.identifier.pmid","30443017"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59754"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/209"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/44"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/339580/EU//MITRAC"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/614765/EU//NEUROMOLANATOMY"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P09: Proteinsortierung in der Synapse: Prinzipien und molekulare Organisation"],["dc.relation.issn","2045-2322"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.relation.workinggroup","RG Rizzoli (Quantitative Synaptology in Space and Time)"],["dc.relation.workinggroup","RG Urlaub (Bioanalytische Massenspektrometrie)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The codon sequences predict protein lifetimes and other parameters of the protein life cycle in the mouse brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2018Journal Article Research Paper
    [["dc.bibliographiccitation.artnumber","4230"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Fornasiero, Eugenio F."],["dc.contributor.author","Mandad, Sunit"],["dc.contributor.author","Wildhagen, Hanna"],["dc.contributor.author","Alevra, Mihai"],["dc.contributor.author","Rammner, Burkhard"],["dc.contributor.author","Keihani, Sarva"],["dc.contributor.author","Opazo, Felipe"],["dc.contributor.author","Urban, Inga"],["dc.contributor.author","Ischebeck, Till"],["dc.contributor.author","Sakib, M. Sadman"],["dc.contributor.author","Fard, Maryam K."],["dc.contributor.author","Kirli, Koray"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Dennerlein, Sven"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Feussner, Ivo"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.date.accessioned","2019-07-09T11:46:03Z"],["dc.date.available","2019-07-09T11:46:03Z"],["dc.date.issued","2018"],["dc.description.abstract","The turnover of brain proteins is critical for organism survival, and its perturbations are linked to pathology. Nevertheless, protein lifetimes have been difficult to obtain in vivo. They are readily measured in vitro by feeding cells with isotopically labeled amino acids, followed by mass spectrometry analyses. In vivo proteins are generated from at least two sources: labeled amino acids from the diet, and non-labeled amino acids from the degradation of pre-existing proteins. This renders measurements difficult. Here we solved this problem rigorously with a workflow that combines mouse in vivo isotopic labeling, mass spectrometry, and mathematical modeling. We also established several independent approaches to test and validate the results. This enabled us to measure the accurate lifetimes of ~3500 brain proteins. The high precision of our data provided a large set of biologically significant observations, including pathway-, organelle-, organ-, or cell-specific effects, along with a comprehensive catalog of extremely long-lived proteins (ELLPs)."],["dc.identifier.doi","10.1038/s41467-018-06519-0"],["dc.identifier.pmid","30315172"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15388"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59372"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/42"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/41"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15611 but duplicate"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/339580/EU//MITRAC"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/614765/EU//NEUROMOLANATOMY"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P09: Proteinsortierung in der Synapse: Prinzipien und molekulare Organisation"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | A03: Dynamische Analyse der Remodellierung der extrazellulären Matrix (ECM) als Mechanismus der Synapsenorganisation und Plastizität"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.relation.workinggroup","RG Rizzoli (Quantitative Synaptology in Space and Time)"],["dc.relation.workinggroup","RG Urlaub (Bioanalytische Massenspektrometrie)"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","573"],["dc.subject.ddc","612"],["dc.title","Precisely measured protein lifetimes in the mouse brain reveal differences across tissues and subcellular fractions."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2022-07-07Journal Article Research Paper
    [["dc.bibliographiccitation.journal","Human Brain Mapping"],["dc.contributor.author","Komorowski, Arkadiusz"],["dc.contributor.author","MurgaÅ¡, Matej"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Singh, Aditya"],["dc.contributor.author","Gryglewski, Gregor"],["dc.contributor.author","Kasper, Siegfried"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lanzenberger, Rupert"],["dc.contributor.author","Goya-Maldonado, Roberto"],["dc.date.accessioned","2022-08-11T12:45:29Z"],["dc.date.available","2022-08-11T12:45:29Z"],["dc.date.issued","2022-07-07"],["dc.description.abstract","The exploration of the spatial relationship between gene expression profiles and task-evoked response patterns known to be altered in neuropsychiatric disorders, for example depression, can guide the development of more targeted therapies. Here, we estimated the correlation between human transcriptome data and two different brain activation maps measured with functional magnetic resonance imaging (fMRI) in healthy subjects. Whole-brain activation patterns evoked during an emotional face recognition task were associated with topological mRNA expression of genes involved in cellular transport. In contrast, fMRI activation patterns related to the acceptance of monetary rewards were associated with genes implicated in cellular localization processes, metabolism, translation, and synapse regulation. An overlap of these genes with risk genes from major depressive disorder genome-wide association studies revealed the involvement of the master regulators TCF4 and PAX6 in emotion and reward processing. Overall, the identification of stable relationships between spatial gene expression profiles and fMRI data may reshape the prospects for imaging transcriptomics studies."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1002/hbm.26001"],["dc.identifier.pmid","35796185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112712"],["dc.language.iso","en"],["dc.relation.eissn","1097-0193"],["dc.relation.issn","1065-9471"],["dc.relation.issn","1097-0193"],["dc.rights","CC BY 4.0"],["dc.title","Regional gene expression patterns are associated with task-specific brain activation during reward and emotion processing measured with functional MRI"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]
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  • 2016Conference Abstract
    [["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Capece, V."],["dc.contributor.author","Lbik, D."],["dc.contributor.author","Mohamed, B."],["dc.contributor.author","Danner, Bernhard Christoph"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Fischer, A."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2018-11-07T10:15:52Z"],["dc.date.available","2018-11-07T10:15:52Z"],["dc.date.issued","2016"],["dc.format.extent","S61"],["dc.identifier.isi","000375417500120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40903"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Of mice and men - a direct comparison of signaling in pressure overload induced hypertrophy and failure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2019Journal Article
    [["dc.bibliographiccitation.firstpage","112"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","RNA Biology"],["dc.bibliographiccitation.lastpage","124"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Samir, Mohamed"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Abdallah, Fatma"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Seehusen, Frauke"],["dc.contributor.author","Geffers, Robert"],["dc.contributor.author","Hussein, Ashraf"],["dc.contributor.author","Ali, Ahmed A. H."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Pessler, Frank"],["dc.date.accessioned","2021-06-01T10:51:12Z"],["dc.date.available","2021-06-01T10:51:12Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1080/15476286.2019.1669879"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86930"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1555-8584"],["dc.relation.issn","1547-6286"],["dc.title","Organ-specific small non-coding RNA responses in domestic (Sudani) ducks experimentally infected with highly pathogenic avian influenza virus (H5N1)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2020Journal Article
    [["dc.bibliographiccitation.firstpage","S6"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","S7"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Komorowski, A."],["dc.contributor.author","Singh, A."],["dc.contributor.author","Vidal, R."],["dc.contributor.author","Murgaš, M."],["dc.contributor.author","Pena-Centeno, T."],["dc.contributor.author","Gryglewski, G."],["dc.contributor.author","Kasper, S."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Lanzenberger, R."],["dc.contributor.author","Goya-Maldonado, R."],["dc.date.accessioned","2021-04-14T08:32:03Z"],["dc.date.available","2021-04-14T08:32:03Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.euroneuro.2020.09.015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83791"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0924-977X"],["dc.title","P.009 MDK gene expression is correlated with human brain activity during acceptance of monetary rewards"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2020Journal Article Research Paper
    [["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Hindmarsh, Vanessa"],["dc.contributor.author","Weber, Frederike"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Torkieh, Setare"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2020-12-10T14:10:26Z"],["dc.date.available","2020-12-10T14:10:26Z"],["dc.date.issued","2020"],["dc.description.abstract","Heart failure is a major health problem worldwide with a significant morbidity and mortality rate. Although studied extensively in animal models, data from patients at the compensated disease stage are lacking. We sampled myocardium biopsies from aortic stenosis patients with compensated hypertrophy and moderate heart failure and used transcriptomics to study the transition to failure. Sequencing and comparative analysis of analogous samples of mice with transverse aortic constriction identified 25 candidate genes with similar regulation in response to pressure overload, reflecting highly conserved molecular processes. The gene cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) is upregulated in the transition to failure in human and mouse and its function is unknown. Homology to ion channel regulatory toxins suggests a role in Ca2+ cycling. CRISPR/Cas9-mediated loss-of-function leads to dysregulated Ca2+ handling in human-induced pluripotent stem cell-derived cardiomyocytes. The downregulation of prohypertrophic, proapoptotic and Ca2+-signaling pathways upon CRISPLD1-KO and its upregulation in the transition to failure implicates a contribution to adverse remodeling. These findings provide new pathophysiological data on Ca2+ regulation in the transition to failure and novel candidate genes with promising potential for therapeutic interventions."],["dc.identifier.doi","10.1007/s00395-020-0784-4"],["dc.identifier.pmid","32146539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70757"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/350"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.title","CRISPLD1: a novel conserved target in the transition to human heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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