Bogeski, Ivan

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Asfaw, Kinfemichael Geressu"],["dc.contributor.author","Liu, Qiong"],["dc.contributor.author","Xu, Xiaolu"],["dc.contributor.author","Manz, Christina"],["dc.contributor.author","Purper, Sabine"],["dc.contributor.author","Eghbalian, Rose"],["dc.contributor.author","Münch, Stephan W."],["dc.contributor.author","Wehl, Ilona"],["dc.contributor.author","Bräse, Stefan"],["dc.contributor.author","Eiche, Elisabeth"],["dc.contributor.author","Hause, Bettina"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Schepers, Ute"],["dc.contributor.author","Riemann, Michael"],["dc.contributor.author","Nick, Peter"],["dc.date.accessioned","2021-04-14T08:24:27Z"],["dc.date.available","2021-04-14T08:24:27Z"],["dc.date.issued","2020"],["dc.description.abstract","Salinity is a serious challenge to global agriculture and threatens human food security. Plant cells can respond to salt stress either by activation of adaptive responses, or by programmed cell death. The mechanisms deciding the respective response are far from understood, but seem to depend on the degree, to which mitochondria can maintain oxidative homeostasis. Using plant PeptoQ, a Trojan Peptoid, as vehicle, it is possible to transport a coenzyme Q10 (CoQ10) derivative into plant mitochondria. We show that salinity stress in tobacco BY-2 cells (Nicotiana tabacum L. cv Bright Yellow-2) can be mitigated by pretreatment with plant PeptoQ with respect to numerous aspects including proliferation, expansion, redox homeostasis, and programmed cell death. We tested the salinity response for transcripts from nine salt-stress related-genes representing different adaptive responses. While most did not show any significant response, the salt response of the transcription factor NtNAC, probably involved in mitochondrial retrograde signaling, was significantly modulated by the plant PeptoQ. Most strikingly, transcripts for the mitochondrial, Mn-dependent Superoxide Dismutase were rapidly and drastically upregulated in presence of the peptoid, and this response was disappearing in presence of salt. The same pattern, albeit at lower amplitude, was seen for the sodium exporter SOS1. The findings are discussed by a model, where plant PeptoQ modulates retrograde signalling to the nucleus leading to a strong expression of mitochondrial SOD, what renders mitochondria more resilient to perturbations of oxidative balance, such that cells escape salt induced cell death and remain viable."],["dc.identifier.doi","10.1038/s41598-020-68491-4"],["dc.identifier.pmid","32665569"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81286"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/118"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.eissn","2045-2322"],["dc.relation.workinggroup","RG Bogeski"],["dc.rights","CC BY 4.0"],["dc.title","A mitochondria-targeted coenzyme Q peptoid induces superoxide dismutase and alleviates salinity stress in plant cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Trautsch, Irina"],["dc.contributor.author","Heta, Eriona"],["dc.contributor.author","Soong, Poh Loong"],["dc.contributor.author","Levent, Elif"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Mayr, Manuel"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2020-12-10T18:44:38Z"],["dc.date.available","2020-12-10T18:44:38Z"],["dc.date.issued","2019"],["dc.description.abstract","Redox signaling affects all aspects of cardiac function and homeostasis. With the development of genetically encoded fluorescent redox sensors, novel tools for the optogenetic investigation of redox signaling have emerged. Here, we sought to develop a human heart muscle model for in-tissue imaging of redox alterations. For this, we made use of (1) the genetically-encoded Grx1-roGFP2 sensor, which reports changes in cellular glutathione redox status (GSH/GSSG), (2) human embryonic stem cells (HES2), and (3) the engineered heart muscle (EHM) technology. We first generated HES2 lines expressing Grx1-roGFP2 in cytosol or mitochondria compartments by TALEN-guided genomic integration. Grx1-roGFP2 sensor localization and function was verified by fluorescence imaging. Grx1-roGFP2 HES2 were then subjected to directed differentiation to obtain high purity cardiomyocyte populations. Despite being able to report glutathione redox potential from cytosol and mitochondria, we observed dysfunctional sarcomerogenesis in Grx1-roGFP2 expressing cardiomyocytes. Conversely, lentiviral transduction of Grx1-roGFP2 in already differentiated HES2-cardiomyocytes and human foreskin fibroblast was possible, without compromising cell function as determined in EHM from defined Grx1-roGFP2-expressing cardiomyocyte and fibroblast populations. Finally, cell-type specific GSH/GSSG imaging was demonstrated in EHM. Collectively, our observations suggests a crucial role for redox signaling in cardiomyocyte differentiation and provide a solution as to how this apparent limitation can be overcome to enable cell-type specific GSH/GSSG imaging in a human heart muscle context."],["dc.identifier.doi","10.3389/fphys.2019.00272"],["dc.identifier.pmid","31024328"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78535"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/265"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/67"],["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 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.eissn","1664-042X"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Bogeski"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Optogenetic Monitoring of the Glutathione Redox State in Engineered Human Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2561"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Gut"],["dc.bibliographiccitation.lastpage","2573"],["dc.bibliographiccitation.volume","71"],["dc.contributor.affiliation","Latif, Muhammad Umair; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Schmidt, Geske Elisabeth; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Mercan, Sercan; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Rahman, Raza; \r\n2\r\nGastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA"],["dc.contributor.affiliation","Gibhardt, Christine Silvia; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Stejerean-Todoran, Ioana; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Reutlinger, Kristina; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Hessmann, Elisabeth; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Singh, Shiv K; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Moeed, Abdul; \r\n4\r\nInstitute for Microbiology and Hygiene, Medical Center-University of Freiburg, Freiburg, Baden-Württemberg, Germany"],["dc.contributor.affiliation","Rehman, Abdul; \r\n5\r\nInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Butt, Umer Javed; \r\n6\r\nClinical Neuroscience, Max-Planck-Institute for Experimental Medicine, Goettingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Bohnenberger, Hanibal; \r\n7\r\nInstitute of Pathology, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Stroebel, Philipp; \r\n7\r\nInstitute of Pathology, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Bremer, Sebastian Christopher; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Neesse, Albrecht; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Bogeski, Ivan; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Ellenrieder, Volker; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.author","Latif, Muhammad Umair"],["dc.contributor.author","Schmidt, Geske Elisabeth"],["dc.contributor.author","Mercan, Sercan"],["dc.contributor.author","Rahman, Raza"],["dc.contributor.author","Gibhardt, Christine Silvia"],["dc.contributor.author","Stejerean-Todoran, Ioana"],["dc.contributor.author","Reutlinger, Kristina"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Moeed, Abdul"],["dc.contributor.author","Rehman, Abdul"],["dc.contributor.author","Butt, Umer Javed"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Bremer, Sebastian Christopher"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Ellenrieder, Volker"],["dc.date.accessioned","2022-12-07T08:25:00Z"],["dc.date.available","2022-12-07T08:25:00Z"],["dc.date.issued","2022-04-01"],["dc.date.updated","2022-12-07T00:46:04Z"],["dc.description.abstract","ObjectivesNon-alcoholic fatty liver disease (NAFLD) can persist in the stage of simple hepatic steatosis or progress to steatohepatitis (NASH) with an increased risk for cirrhosis and cancer. We examined the mechanisms controlling the progression to severe NASH in order to develop future treatment strategies for this disease.DesignNFATc1 activation and regulation was examined in livers from patients with NAFLD, cultured and primary hepatocytes and in transgenic mice with differential hepatocyte-specific expression of the transcription factor (Alb-cre, NFATc1c.a\r\n. and NFATc1Δ/Δ\r\n). Animals were fed with high-fat western diet (WD) alone or in combination with tauroursodeoxycholic acid (TUDCA), a candidate drug for NAFLD treatment. NFATc1-dependent ER stress-responses, NLRP3 inflammasome activation and disease progression were assessed both in vitro and in vivo.ResultsNFATc1 expression was weak in healthy livers but strongly induced in advanced NAFLD stages, where it correlates with liver enzyme values as well as hepatic inflammation and fibrosis. Moreover, high-fat WD increased NFATc1 expression, nuclear localisation and activation to promote NAFLD progression, whereas hepatocyte-specific depletion of the transcription factor can prevent mice from disease acceleration. Mechanistically, NFATc1 drives liver cell damage and inflammation through ER stress sensing and activation of the PERK-CHOP unfolded protein response (UPR). Finally, NFATc1-induced disease progression towards NASH can be blocked by TUDCA administration.ConclusionNFATc1 stimulates NAFLD progression through chronic ER stress sensing and subsequent activation of terminal UPR signalling in hepatocytes. Interfering with ER stress-responses, for example, by TUDCA, protects fatty livers from progression towards manifest NASH."],["dc.description.sponsorship","the Volkswagen-Stiftung"],["dc.description.sponsorship","http://dx.doi.org/10.13039/501100001659Deutsche Forschungsgemeinschaft"],["dc.description.sponsorship","German Cancer Aid"],["dc.identifier","35365570"],["dc.identifier.doi","10.1136/gutjnl-2021-325013"],["dc.identifier.pmid","35365570"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118455"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/173"],["dc.language.iso","en"],["dc.publisher","BMJ Publishing Group Ltd and British Society of Gastroenterology"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.eissn","1468-3288"],["dc.relation.issn","0017-5749"],["dc.relation.workinggroup","RG Bogeski"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc/4.0/"],["dc.title","NFATc1 signaling drives chronic ER stress responses to promote NAFLD progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["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.firstpage","642"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Metabolism"],["dc.bibliographiccitation.lastpage","653.e6"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Pak, Valeriy V."],["dc.contributor.author","Ezeriņa, Daria"],["dc.contributor.author","Lyublinskaya, Olga G."],["dc.contributor.author","Pedre, Brandán"],["dc.contributor.author","Tyurin-Kuzmin, Pyotr A."],["dc.contributor.author","Mishina, Natalie M."],["dc.contributor.author","Thauvin, Marion"],["dc.contributor.author","Young, David"],["dc.contributor.author","Wahni, Khadija"],["dc.contributor.author","Martínez Gache, Santiago Agustín"],["dc.contributor.author","Demidovich, Alexandra D."],["dc.contributor.author","Ermakova, Yulia G."],["dc.contributor.author","Maslova, Yulia D."],["dc.contributor.author","Shokhina, Arina G."],["dc.contributor.author","Eroglu, Emrah"],["dc.contributor.author","Bilan, Dmitry S."],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Michel, Thomas"],["dc.contributor.author","Vriz, Sophie"],["dc.contributor.author","Messens, Joris"],["dc.contributor.author","Belousov, Vsevolod V."],["dc.date.accessioned","2020-12-10T14:23:10Z"],["dc.date.available","2020-12-10T14:23:10Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.cmet.2020.02.003"],["dc.identifier.pmid","32130885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71855"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/109"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.workinggroup","RG Bogeski"],["dc.title","Ultrasensitive Genetically Encoded Indicator for Hydrogen Peroxide Identifies Roles for the Oxidant in Cell Migration and Mitochondrial Function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","11"],["dc.bibliographiccitation.journal","Free Radical Biology and Medicine"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Bogeski, Ivan"],["dc.date.accessioned","2020-12-10T14:24:11Z"],["dc.date.available","2020-12-10T14:24:11Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.freeradbiomed.2017.10.362"],["dc.identifier.issn","0891-5849"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72173"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Redox Regulation Of Ca 2+ Channels: From Orai To MCU"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","138"],["dc.bibliographiccitation.journal","Current Opinion in Physiology"],["dc.bibliographiccitation.lastpage","148"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Gibhardt, Christine S."],["dc.contributor.author","Ezeriņa, Daria"],["dc.contributor.author","Sung, Hsu-Min"],["dc.contributor.author","Messens, Joris"],["dc.contributor.author","Bogeski, Ivan"],["dc.date.accessioned","2022-07-11T15:36:50Z"],["dc.date.available","2022-07-11T15:36:50Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.cophys.2020.07.017"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112470"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/125"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.issn","2468-8673"],["dc.relation.workinggroup","RG Bogeski"],["dc.title","Redox regulation of the mitochondrial calcium transport machinery"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","501"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Antioxidants & Redox Signaling"],["dc.bibliographiccitation.lastpage","517"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Bozem, Monika"],["dc.contributor.author","Knapp, Phillip"],["dc.contributor.author","Mirčeski, Valentin"],["dc.contributor.author","Slowik, Ewa J."],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Kappl, Reinhard"],["dc.contributor.author","Heinemann, Christian"],["dc.contributor.author","Hoth, Markus"],["dc.date.accessioned","2020-12-10T18:16:01Z"],["dc.date.available","2020-12-10T18:16:01Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1089/ars.2016.6840"],["dc.identifier.eissn","1557-7716"],["dc.identifier.issn","1523-0864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75023"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Electrochemical Quantification of Extracellular Local H 2 O 2 Kinetics Originating from Single Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e79125"],["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Shumanska, Magdalena"],["dc.contributor.author","Bogeski, Ivan"],["dc.date.accessioned","2022-06-01T09:40:05Z"],["dc.date.available","2022-06-01T09:40:05Z"],["dc.date.issued","2022"],["dc.description.abstract","The oxidative state of a critical cysteine residue determines the enzymatic activity of a phosphatase involved in T-cell immune responses."],["dc.identifier.doi","10.7554/eLife.79125"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108632"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2050-084X"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Redoxing PTPN22 activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","183"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.seriesnr","1925"],["dc.contributor.author","Gibhardt, Christine S."],["dc.contributor.author","Vultur, Adina"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.editor","Raffaello, Anna"],["dc.contributor.editor","Vecellio Reane, Denis"],["dc.date.accessioned","2021-06-02T10:44:26Z"],["dc.date.available","2021-06-02T10:44:26Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/978-1-4939-9018-4_17"],["dc.identifier.pmid","30674028"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87038"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/82"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","Springer New York"],["dc.publisher.place","New York, NY"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.crisseries","Methods in Molecular Biology"],["dc.relation.eisbn","978-1-4939-9018-4"],["dc.relation.isbn","978-1-4939-9017-7"],["dc.relation.ispartof","Methods in Molecular Biology"],["dc.relation.ispartof","Calcium Signalling : Methods and Protocols"],["dc.relation.ispartofseries","Methods in Molecular Biology; 1925"],["dc.relation.workinggroup","RG Bogeski"],["dc.title","Measuring Calcium and ROS by Genetically Encoded Protein Sensors and Fluorescent Dyes"],["dc.type","book_chapter"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]