Streckfuß-Bömeke, Katrin

[["dc.bibliographiccitation.firstpage","909"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Molecular Biology"],["dc.bibliographiccitation.lastpage","925"],["dc.bibliographiccitation.volume","405"],["dc.contributor.author","Herzog, Britta"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2018-11-07T09:00:02Z"],["dc.date.available","2018-11-07T09:00:02Z"],["dc.date.issued","2011"],["dc.description.abstract","The basic zipper Gcn4 protein activates transcription in the yeast Saccharomyces cerevisiae in response to amino acid starvation. This includes numerous metabolic genes of amino acid or purine biosynthesis and the developmental cell-surface flocculin gene FLO11, which is required for diploid pseudohyphae formation and for adhesion upon nutrient starvation. We separated the metabolic from the developmental response by screening for GCN4 alleles that allow growth during amino acid starvation but are impaired in adhesion and are unable to form pseudohyphae. The identified Gcn4(L267S) variant carries an amino acid substitution in the third of the four conserved leucines of the zipper dimerization domain. This mutation abolished FLO11 expression and results in reduced but sufficient transcriptional activity for amino acid biosynthetic genes. The Leu267Ser substitution impairs Gcn4 homodimer formation and is a significantly more stable protein than the wild-type protein. A helix-breaker substitution in Leu253 results in a transcriptionally inactive but highly stable protein variant. This is due to a feedback circuit between transcriptional activity of Gcn4 and its own stability, which depends on the Gcn4-controlled cyclin PCL5. Gcn4(L253G) reduces the expression of Pcl5 and therefore reduces its own degradation. This self-controlled buffer system to restrict transcriptional activity results in a reciprocal correlation between Gcn4 transcriptional activity and protein stability. (C) 2010 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.jmb.2010.11.033"],["dc.identifier.isi","000286962300003"],["dc.identifier.pmid","21111745"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24051"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","0022-2836"],["dc.title","A Feedback Circuit between Transcriptional Activation and Self-Destruction of Gcn4 Separates Its Metabolic and Morphogenic Response in Diploid Yeasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","139"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Vlasov, Alla"],["dc.contributor.author","Huelsmann, Swen"],["dc.contributor.author","Yin, Dongjiao"],["dc.contributor.author","Nayernia, Karim"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2017-09-07T11:47:33Z"],["dc.date.available","2017-09-07T11:47:33Z"],["dc.date.issued","2009"],["dc.description.abstract","Recently, we reported the successful establishment of multipotent adult germ-Line stem cells (maGSCs) from cultured adult mouse spermatogonial stem cells. Similar to embryonic stem cells, maGSCs are able to self-renew and differentiate into derivatives of all three germ Layers. These properties make maGSCs a potential cell source for the treatment of neural degenerative diseases. In this study, we describe the generation of maGSC-derived proliferating neural precursor cells using growth factor-mediated neural Lineage induction. The neural precursors were positive for nestin and Sox1 and could be continuously expanded. Upon further differentiation, they formed functional neurons and glial cells, as demonstrated by expression of lineage-restricted genes and proteins and by electrophysiological properties. Characterization of maGSC-derived neurons revealed the generation of specific subtypes, including GABAergic, glutamatergic, serotonergic, and dopaminergic neurons. Electrophysiological analysis revealed passive and active membrane properties and postsynaptic currents, indicating their functional maturation. Functional networks formed at later stages of differentiation, as evidenced by synaptic transmission of spontaneous neuronal activity. In conclusion, our data demonstrate that maGSCs may be used as a new stem cell source for basic research and biomedical. applications. (C) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.scr.2008.09.001"],["dc.identifier.gro","3143148"],["dc.identifier.isi","000272224500006"],["dc.identifier.pmid","19383419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/630"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-5061"],["dc.title","Generation of functional neurons and glia from multipotent adult mouse germ-line stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e202000987"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Life Science Alliance"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Sargsyan, Yelena"],["dc.contributor.author","Bickmeyer, Uta"],["dc.contributor.author","Gibhardt, Christine S"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Thoms, Sven"],["dc.date.accessioned","2021-08-12T07:45:41Z"],["dc.date.available","2021-08-12T07:45:41Z"],["dc.date.issued","2021"],["dc.description.abstract","Peroxisomes communicate with other cellular compartments by transfer of various metabolites. However, whether peroxisomes are sites for calcium handling and exchange has remained contentious. Here we generated sensors for assessment of peroxisomal calcium and applied them for single cell-based calcium imaging in HeLa cells and cardiomyocytes. We found that peroxisomes in HeLa cells take up calcium upon depletion of intracellular calcium stores and upon calcium influx across the plasma membrane. Furthermore, we show that peroxisomes of neonatal rat cardiomyocytes and human induced pluripotent stem cell–derived cardiomyocytes can take up calcium. Our results indicate that peroxisomal and cytosolic calcium signals are tightly interconnected both in HeLa cells and in cardiomyocytes. Cardiac peroxisomes take up calcium on beat-to-beat basis. Hence, peroxisomes may play an important role in shaping cellular calcium dynamics of cardiomyocytes."],["dc.description.abstract","Peroxisomes communicate with other cellular compartments by transfer of various metabolites. However, whether peroxisomes are sites for calcium handling and exchange has remained contentious. Here we generated sensors for assessment of peroxisomal calcium and applied them for single cell-based calcium imaging in HeLa cells and cardiomyocytes. We found that peroxisomes in HeLa cells take up calcium upon depletion of intracellular calcium stores and upon calcium influx across the plasma membrane. Furthermore, we show that peroxisomes of neonatal rat cardiomyocytes and human induced pluripotent stem cell–derived cardiomyocytes can take up calcium. Our results indicate that peroxisomal and cytosolic calcium signals are tightly interconnected both in HeLa cells and in cardiomyocytes. Cardiac peroxisomes take up calcium on beat-to-beat basis. Hence, peroxisomes may play an important role in shaping cellular calcium dynamics of cardiomyocytes."],["dc.identifier.doi","10.26508/lsa.202000987"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88529"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","2575-1077"],["dc.title","Peroxisomes contribute to intracellular calcium dynamics in cardiomyocytes and non-excitable cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Fischer, C."],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Perret, A."],["dc.contributor.author","Oezcelic, C."],["dc.contributor.author","Wagner, S."],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2018-11-07T09:37:39Z"],["dc.date.available","2018-11-07T09:37:39Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1093/cvr/cvu083.2"],["dc.identifier.isi","000343730100211"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32886"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.title","RBM20-dependent regulation of organized myofilament structure and titin splicing in induced pluripotent stem cell-derived cardiomyocytes from patients with dilative cardiomyopathy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","496"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Eukaryotic Cell"],["dc.bibliographiccitation.lastpage","510"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Schulze, Florian"],["dc.contributor.author","Herzog, Britta"],["dc.contributor.author","Scholz, Eva"],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2018-11-07T08:31:01Z"],["dc.date.available","2018-11-07T08:31:01Z"],["dc.date.issued","2009"],["dc.description.abstract","Pcl5 is a Saccharomyces cerevisiae cyclin that directs the phosphorylation of the general amino acid control transcriptional activator Gcn4 by the cyclin-dependent kinase (CDK) Pho85. Phosphorylation of Gcn4 by Pho85/Pcl5 initiates its degradation via the ubiquitin/proteasome system and is regulated by the availability of amino acids. In this study, we show that Pcl5 is a nuclear protein and that artificial dislocation of Pcl5 into the cytoplasm prevents the degradation of Gcn4. Nuclear localization of Pcl5 depends on the beta-importin Kap95 and does not require Pho85, Gcn4, or the CDK inhibitor Pho81. Pcl5 nuclear import is independent on the availability of amino acids and is mediated by sequences in its C-terminal domain. The nuclear localization signal is distinct from other functional domains of Pcl5. This is corroborated by a C-terminally truncated Pcl5 variant, which carries the N-terminal nuclear domain of Pho80. This hybrid is still able to fulfill Pcl5 function, whereas Pho80, which is another Pho85 interacting cyclin, does not mediate Gcn4 degradation."],["dc.identifier.doi","10.1128/EC.00324-08"],["dc.identifier.isi","000265041800011"],["dc.identifier.pmid","19218424"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17025"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","1535-9778"],["dc.title","Degradation of Saccharomyces cerevisiae Transcription Factor Gcn4 Requires a C-Terminal Nuclear Localization Signal in the Cyclin Pcl5"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","272"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","273"],["dc.bibliographiccitation.volume","269"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2020-12-10T14:24:32Z"],["dc.date.available","2020-12-10T14:24:32Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.ijcard.2018.07.101"],["dc.identifier.issn","0167-5273"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72286"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Clinical nuclear medicine tracers: Easy metabolic assays in stem cell research and cardiac disease?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1690"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","1700"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Bollenberg, Hannah"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Kovács, Árpád"],["dc.contributor.author","Schach, Christian"],["dc.contributor.author","Tirilomis, Petros"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Renner, André"],["dc.contributor.author","Gummert, Jan"],["dc.contributor.author","Fischer, Thomas"],["dc.contributor.author","Van Linthout, Sophie"],["dc.contributor.author","Tschöpe, Carsten"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2019-02-19T13:12:22Z"],["dc.date.available","2019-02-19T13:12:22Z"],["dc.date.issued","2018"],["dc.description.abstract","Aims Empagliflozin, a clinically used oral antidiabetic drug that inhibits the sodium-dependent glucose co-transporter 2, has recently been evaluated for its cardiovascular safety. Surprisingly, empagliflozin reduced mortality and hospitalization for heart failure (HF) compared to placebo. However, the underlying mechanisms remain unclear. Therefore, our study aims to investigate whether empagliflozin may cause direct pleiotropic effects on the myocardium. Methods and results In order to assess possible direct myocardial effects of empagliflozin, we performed contractility experiments with in toto-isolated human systolic end-stage HF ventricular trabeculae. Empagliflozin significantly reduced diastolic tension, whereas systolic force was not changed. These results were confirmed in murine myocardium from diabetic and non-diabetic mice, suggesting independent effects from diabetic conditions. In human HF cardiomyocytes, empagliflozin did not influence calcium transient amplitude or diastolic calcium level. The mechanisms underlying the improved diastolic function were further elucidated by studying myocardial fibres from patients and rats with diastolic HF (HF with preserved ejection fraction, HFpEF). Empagliflozin beneficially reduced myofilament passive stiffness by enhancing phosphorylation levels of myofilament regulatory proteins. Intravenous injection of empagliflozin in anaesthetized HFpEF rats significantly improved diastolic function measured by echocardiography, while systolic contractility was unaffected. Conclusion Empagliflozin causes direct pleiotropic effects on the myocardium by improving diastolic stiffness and hence diastolic function. These effects were independent of diabetic conditions. Since pharmacological therapy of diastolic dysfunction and HF is an unmet need, our results provide a rationale for new translational studies and might also contribute to the understanding of the EMPA-REG OUTCOME trial."],["dc.identifier.doi","10.1002/ejhf.1328"],["dc.identifier.pmid","30328645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57583"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/239"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A11: Absolute Arrhythmie bei Vorhofflimmern - ein neuer Mechanismus, der zu einer Störung von Ca2+-Homöostase und elektrischer Stabilität in der Transition zur Herzinsuffizienz führt"],["dc.relation.issn","1879-0844"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG T. Fischer"],["dc.title","Empagliflozin directly improves diastolic function in human heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Haupt, Luis Peter"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Maurer, Wiebke"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Maus, Andreas"],["dc.contributor.author","Köhne, Steffen"],["dc.contributor.author","Tappu, Rewati"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2022-04-01T10:01:09Z"],["dc.date.available","2022-04-01T10:01:09Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Cancer therapies with anthracyclines have been shown to induce cardiovascular complications. The aims of this study were to establish an in vitro induced pluripotent stem cell model (iPSC) of anthracycline-induced cardiotoxicity (ACT) from patients with an aggressive form of B-cell lymphoma and to examine whether doxorubicin (DOX)-treated ACT-iPSC cardiomyocytes (CM) can recapitulate the clinical features exhibited by patients, and thus help uncover a DOX-dependent pathomechanism. ACT-iPSC CM generated from individuals with CD20 + B-cell lymphoma who had received high doses of DOX and suffered cardiac dysfunction were studied and compared to control-iPSC CM from cancer survivors without cardiac symptoms. In cellular studies, ACT-iPSC CM were persistently more susceptible to DOX toxicity including augmented disorganized myofilament structure, changed mitochondrial shape, and increased apoptotic events. Consistently, ACT-iPSC CM and cardiac fibroblasts isolated from fibrotic human ACT myocardium exhibited higher DOX-dependent reactive oxygen species. In functional studies, Ca 2+ transient amplitude of ACT-iPSC CM was reduced compared to control cells, and diastolic sarcoplasmic reticulum Ca 2+ leak was DOX-dependently increased. This could be explained by overactive CaMKIIδ in ACT CM. Together with DOX-dependent augmented proarrhythmic cellular triggers and prolonged action potentials in ACT CM, this suggests a cellular link to arrhythmogenic events and contractile dysfunction especially found in ACT engineered human myocardium. CamKIIδ inhibition prevented proarrhythmic triggers in ACT. In contrast, control CM upregulated SERCA2a expression in a DOX-dependent manner, possibly to avoid heart failure conditions. In conclusion, we developed the first human patient-specific stem cell model of DOX-induced cardiac dysfunction from patients with B-cell lymphoma. Our results suggest that DOX-induced stress resulted in arrhythmogenic events associated with contractile dysfunction and finally in heart failure after persistent stress activation in ACT patients."],["dc.identifier.doi","10.1007/s00395-022-00918-7"],["dc.identifier.pii","918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105613"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1435-1803"],["dc.relation.issn","0300-8428"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Doxorubicin induces cardiotoxicity in a pluripotent stem cell model of aggressive B cell lymphoma cancer patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Human Gene Therapy"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Wolf, F."],["dc.contributor.author","Becker, A."],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Huebscher, Daniela"],["dc.contributor.author","Field, Loren J."],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2018-11-07T11:22:43Z"],["dc.date.available","2018-11-07T11:22:43Z"],["dc.date.issued","2009"],["dc.format.extent","1406"],["dc.identifier.isi","000271441000171"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56035"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mary Ann Liebert Inc"],["dc.publisher.place","New rochelle"],["dc.relation.conference","Combined Meeting of the 17th European-Society-of-Gene-and-Cell-Therapy/16th German-Society-for-Gene-Therapy/4th German-Society-for-Stem-Cell-Research"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","1043-0342"],["dc.title","Characterization and maintenance of adult spermatogonial stem cell culture"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","S1873506122000265"],["dc.bibliographiccitation.firstpage","102677"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Maurer, Wiebke"],["dc.contributor.author","Hartmann, Nico"],["dc.contributor.author","Argyriou, Loukas"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2022-06-01T09:39:00Z"],["dc.date.available","2022-06-01T09:39:00Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/j.scr.2022.102677"],["dc.identifier.pii","S1873506122000265"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108363"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.issn","1873-5061"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Generation of homozygous Nav1.8 knock-out iPSC lines by CRISPR Cas9 genome editing to investigate a potential new antiarrhythmic strategy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]