Bogeski, Ivan

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Klein, Marie-Christine"],["dc.contributor.author","Zimmermann, Katharina"],["dc.contributor.author","Schorr, Stefan"],["dc.contributor.author","Landini, Martina"],["dc.contributor.author","Klemens, Patrick A. W."],["dc.contributor.author","Altensell, Jacqueline"],["dc.contributor.author","Jung, Martin"],["dc.contributor.author","Krause, Elmar"],["dc.contributor.author","Nguyen, Duy"],["dc.contributor.author","Helms, Volkhard"],["dc.contributor.author","Rettig, Jens"],["dc.contributor.author","Fecher-Trost, Claudia"],["dc.contributor.author","Cavalié, Adolfo"],["dc.contributor.author","Hoth, Markus"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Neuhaus, H. Ekkehard"],["dc.contributor.author","Zimmermann, Richard"],["dc.contributor.author","Lang, Sven"],["dc.contributor.author","Haferkamp, Ilka"],["dc.date.accessioned","2020-12-10T18:09:48Z"],["dc.date.available","2020-12-10T18:09:48Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41467-018-06003-9"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15608"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73762"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/39"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["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.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","AXER is an ATP/ADP exchanger in the membrane of the endoplasmic reticulum"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e100871"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Zhang, Xin"],["dc.contributor.author","Gibhardt, Christine S"],["dc.contributor.author","Will, Thorsten"],["dc.contributor.author","Stanisz, Hedwig"],["dc.contributor.author","Körbel, Christina"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Stejerean, Ioana"],["dc.contributor.author","Cappello, Sabrina"],["dc.contributor.author","Pacheu-Grau, David"],["dc.contributor.author","Dudek, Jan"],["dc.contributor.author","Tahbaz, Nasser"],["dc.contributor.author","Mina, Lucas"],["dc.contributor.author","Simmen, Thomas"],["dc.contributor.author","Laschke, Matthias W"],["dc.contributor.author","Menger, Michael D"],["dc.contributor.author","Schön, Michael P"],["dc.contributor.author","Helms, Volkhard"],["dc.contributor.author","Niemeyer, Barbara A"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Vultur, Adina"],["dc.contributor.author","Bogeski, Ivan"],["dc.date.accessioned","2020-04-29T13:50:36Z"],["dc.date.available","2020-04-29T13:50:36Z"],["dc.date.issued","2019"],["dc.description.abstract","Reactive oxygen species (ROS) are emerging as important regulators of cancer growth and metastatic spread. However, how cells integrate redox signals to affect cancer progression is not fully understood. Mitochondria are cellular redox hubs, which are highly regulated by interactions with neighboring organelles. Here, we investigated how ROS at the endoplasmic reticulum (ER)-mitochondria interface are generated and translated to affect melanoma outcome. We show that TMX1 and TMX3 oxidoreductases, which promote ER-mitochondria communication, are upregulated in melanoma cells and patient samples. TMX knockdown altered mitochondrial organization, enhanced bioenergetics, and elevated mitochondrial- and NOX4-derived ROS. The TMX-knockdown-induced oxidative stress suppressed melanoma proliferation, migration, and xenograft tumor growth by inhibiting NFAT1. Furthermore, we identified NFAT1-positive and NFAT1-negative melanoma subgroups, wherein NFAT1 expression correlates with melanoma stage and metastatic potential. Integrative bioinformatics revealed that genes coding for mitochondrial- and redox-related proteins are under NFAT1 control and indicated that TMX1, TMX3, and NFAT1 are associated with poor disease outcome. Our study unravels a novel redox-controlled ER-mitochondria-NFAT1 signaling loop that regulates melanoma pathobiology and provides biomarkers indicative of aggressive disease."],["dc.identifier.doi","10.15252/embj.2018100871"],["dc.identifier.pmid","31304984"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16534"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64486"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/80"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P13: Protein Transport über den mitochondrialen Carrier Transportweg"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.eissn","1460-2075"],["dc.relation.issn","0261-4189"],["dc.relation.issn","1460-2075"],["dc.relation.workinggroup","RG Bogeski"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Redox signals at the ER-mitochondria interface control melanoma 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.artnumber","44357"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Zhou, X."],["dc.contributor.author","Zhao, Renping"],["dc.contributor.author","Schwarz, Karsten"],["dc.contributor.author","Mangeat, Matthieu"],["dc.contributor.author","Schwarz, Eva C."],["dc.contributor.author","Hamed, Mohamed"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Helms, Volkhard"],["dc.contributor.author","Rieger, Heiko"],["dc.contributor.author","Qu, Bin"],["dc.date.accessioned","2018-11-07T10:26:13Z"],["dc.date.available","2018-11-07T10:26:13Z"],["dc.date.issued","2017"],["dc.description.abstract","Natural killer (NK) cells play a central role during innate immune responses by eliminating pathogen-infected or tumorigenic cells. In the microenvironment, NK cells encounter not only target cells but also other cell types including non-target bystander cells. The impact of bystander cells on NK killing efficiency is, however, still elusive. In this study we show that the presence of bystander cells, such as P815, monocytes or HUVEC, enhances NK killing efficiency. With bystander cells present, the velocity and persistence of NK cells were increased, whereas the degranulation of lytic granules remained unchanged. Bystander cell-derived H2O2 was found to mediate the acceleration of NK cell migration. Using mathematical diffusion models, we confirm that local acceleration of NK cells in the vicinity of bystander cells reduces their search time to locate target cells. In addition, we found that integrin beta chains (beta 1, beta 2 and beta 7) on NK cells are required for bystander-enhanced NK migration persistence. In conclusion, we show that acceleration of NK cell migration in the vicinity of H2O2-producing bystander cells reduces target cell search time and enhances NK killing efficiency."],["dc.description.sponsorship","DFG [INST 256/419-1 FUGG]; [Sonderforschungsbereich 1027]"],["dc.identifier.doi","10.1038/srep44357"],["dc.identifier.isi","000396212400001"],["dc.identifier.pmid","28287155"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14934"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42994"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Bystander cells enhance NK cytotoxic efficiency by reducing search time"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]