Lodygin, Dmitri

[["dc.bibliographiccitation.firstpage","eabd5647"],["dc.bibliographiccitation.issue","675"],["dc.bibliographiccitation.journal","Science Signaling"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Roggenkamp, Hannes G."],["dc.contributor.author","Khansahib, Imrankhan"],["dc.contributor.author","Hernandez C., Lola C."],["dc.contributor.author","Zhang, Yunpeng"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Krüger, Aileen"],["dc.contributor.author","Gu, Feng"],["dc.contributor.author","Möckl, Franziska"],["dc.contributor.author","Löhndorf, Anke"],["dc.contributor.author","Wolters, Valerie"],["dc.contributor.author","Woike, Daniel"],["dc.contributor.author","Rosche, Anette"],["dc.contributor.author","Bauche, Andreas"],["dc.contributor.author","Schetelig, Daniel"],["dc.contributor.author","Werner, René"],["dc.contributor.author","Schlüter, Hartmut"],["dc.contributor.author","Failla, Antonio V."],["dc.contributor.author","Meier, Chris"],["dc.contributor.author","Fliegert, Ralf"],["dc.contributor.author","Walseth, Timothy F."],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Diercks, Björn-Philipp"],["dc.contributor.author","Guse, Andreas H."],["dc.date.accessioned","2021-04-14T08:28:14Z"],["dc.date.available","2021-04-14T08:28:14Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1126/scisignal.abd5647"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82545"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1937-9145"],["dc.relation.issn","1945-0877"],["dc.title","HN1L/JPT2: A signaling protein that connects NAADP generation to Ca 2+ microdomain formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","eaat0358"],["dc.bibliographiccitation.issue","561"],["dc.bibliographiccitation.journal","Science Signaling"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Diercks, Björn-Philipp"],["dc.contributor.author","Werner, René"],["dc.contributor.author","Weidemüller, Paula"],["dc.contributor.author","Czarniak, Frederik"],["dc.contributor.author","Hernandez, Lola"],["dc.contributor.author","Lehmann, Cari"],["dc.contributor.author","Rosche, Annette"],["dc.contributor.author","Krüger, Aileen"],["dc.contributor.author","Kaufmann, Ulrike"],["dc.contributor.author","Vaeth, Martin"],["dc.contributor.author","Failla, Antonio V."],["dc.contributor.author","Zobiak, Bernd"],["dc.contributor.author","Kandil, Farid I."],["dc.contributor.author","Schetelig, Daniel"],["dc.contributor.author","Ruthenbeck, Alexandra"],["dc.contributor.author","Meier, Chris"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Ren, Dejian"],["dc.contributor.author","Wolf, Insa M. A."],["dc.contributor.author","Feske, Stefan"],["dc.contributor.author","Guse, Andreas H."],["dc.date.accessioned","2020-12-10T18:36:46Z"],["dc.date.available","2020-12-10T18:36:46Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1126/scisignal.aat0358"],["dc.identifier.eissn","1937-9145"],["dc.identifier.issn","1945-0877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76733"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","ORAI1, STIM1/2, and RYR1 shape subsecond Ca 2+ microdomains upon T cell activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","ra102"],["dc.bibliographiccitation.issue","398"],["dc.bibliographiccitation.journal","Science Signaling"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Wolf, Insa M. A."],["dc.contributor.author","Diercks, Bjoern-Philipp"],["dc.contributor.author","Gattkowski, Ellen"],["dc.contributor.author","Czarniak, Frederik"],["dc.contributor.author","Kempski, Jan"],["dc.contributor.author","Werner, Rene"],["dc.contributor.author","Schetelig, Daniel"],["dc.contributor.author","Mittrücker, Hans-Willi"],["dc.contributor.author","Schumacher, Valea"],["dc.contributor.author","von Osten, Manuel"],["dc.contributor.author","Lodygin, Dimitri"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Fliegert, Ralf"],["dc.contributor.author","Guse, Andreas H."],["dc.date.accessioned","2018-11-07T09:50:15Z"],["dc.date.available","2018-11-07T09:50:15Z"],["dc.date.issued","2015"],["dc.description.abstract","The activation of T cells is the fundamental on switch for the adaptive immune system. Ca2+ signaling is essential for T cell activation and starts as initial, short-lived, localized Ca2+ signals. The second messenger nicotinic acid adenine dinucleotide phosphate (NAADP) forms rapidly upon T cell activation and stimulates early Ca2+ signaling. We developed a high-resolution imaging technique using multiple fluorescent Ca2+ indicator dyes to characterize these early signaling events and investigate the channels involved in NAADP-dependent Ca2+ signals. In the first seconds of activation of either primary murine T cells or human Jurkat cells with beads coated with an antibody against CD3, we detected Ca2+ signals with diameters close to the limit of detection and that were close to the activation site at the plasma membrane. In Jurkat cells in which the ryanodine receptor (RyR) was knocked down or in primary T cells from RyR1(-/-) mice, either these early Ca2+ signals were not detected or the number of signals was markedly reduced. Local Ca2+ signals observed within 20 ms upon microinjection of Jurkat cells with NAADP were also sensitive to RyR knockdown. In contrast, TRPM2 (transient receptor potential channel, subtype melastatin 2), a potential NAADP target channel, was not required for the formation of initial Ca2+ signals in primary T cells. Thus, through our high-resolution imaging method, we characterized early Ca2+ release events in T cells and obtained evidence for the involvement of RyR and NAADP in such signals."],["dc.identifier.doi","10.1126/scisignal.aab0863"],["dc.identifier.isi","000363319600002"],["dc.identifier.pmid","26462735"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35676"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1937-9145"],["dc.relation.issn","1945-0877"],["dc.title","Frontrunners of T cell activation: Initial, localized Ca2+ signals mediated by NAADP and the type 1 ryanodine receptor"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","709"],["dc.bibliographiccitation.journal","Science Signaling"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Gu, Feng"],["dc.contributor.author","Krüger, Aileen"],["dc.contributor.author","Roggenkamp, Hannes G."],["dc.contributor.author","Alpers, Rick"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Jaquet, Vincent"],["dc.contributor.author","Möckl, Franziska"],["dc.contributor.author","Hernandez C., Lola C."],["dc.contributor.author","Winterberg, Kai"],["dc.contributor.author","Bauche, Andreas"],["dc.contributor.author","Guse, Andreas H."],["dc.date.accessioned","2021-12-01T09:21:16Z"],["dc.date.available","2021-12-01T09:21:16Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1126/scisignal.abe3800"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94393"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1937-9145"],["dc.relation.issn","1945-0877"],["dc.title","Dual NADPH oxidases DUOX1 and DUOX2 synthesize NAADP and are necessary for Ca 2+ signaling during T cell activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1930"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1943"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Cordiglieri, Chiara"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Zhang, B. O."],["dc.contributor.author","Nebel, Merle"],["dc.contributor.author","Kawakami, Naoto"],["dc.contributor.author","Klinkert, Wolfgang E. F."],["dc.contributor.author","Lodygin, Dimtri"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Breunig, Esther"],["dc.contributor.author","Schild, Detlev"],["dc.contributor.author","Ulaganathan, Vijay Kumar"],["dc.contributor.author","Dornmair, Klaus"],["dc.contributor.author","Dammermann, Werner"],["dc.contributor.author","Potter, Barry V. L."],["dc.contributor.author","Guse, Andreas H."],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T08:41:30Z"],["dc.date.available","2018-11-07T08:41:30Z"],["dc.date.issued","2010"],["dc.description.abstract","Nicotinic acid adenine dinucleotide phosphate represents a newly identified second messenger in T cells involved in antigen receptor-mediated calcium signalling. Its function in vivo is, however, unknown due to the lack of biocompatible inhibitors. Using a recently developed inhibitor, we explored the role of nicotinic acid adenine dinucleotide phosphate in autoreactive effector T cells during experimental autoimmune encephalomyelitis, the animal model for multiple sclerosis. We provide in vitro and in vivo evidence that calcium signalling controlled by nicotinic acid adenine dinucleotide phosphate is relevant for the pathogenic potential of autoimmune effector T cells. Live two photon imaging and molecular analyses revealed that nicotinic acid adenine dinucleotide phosphate signalling regulates T cell motility and re-activation upon arrival in the nervous tissues. Treatment with the nicotinic acid adenine dinucleotide phosphate inhibitor significantly reduced both the number of stable arrests of effector T cells and their invasive capacity. The levels of pro-inflammatory cytokines interferon-gamma and interleukin-17 were strongly diminished. Consecutively, the clinical symptoms of experimental autoimmune encephalomyelitis were ameliorated. In vitro, antigen-triggered T cell proliferation and cytokine production were evenly suppressed. These inhibitory effects were reversible: after wash-out of the nicotinic acid adenine dinucleotide phosphate antagonist, the effector T cells fully regained their functions. The nicotinic acid derivative BZ194 induced this transient state of non-responsiveness specifically in post-activated effector T cells. Naive and long-lived memory T cells, which express lower levels of the putative nicotinic acid adenine dinucleotide phosphate receptor, type 1 ryanodine receptor, were not targeted. T cell priming and recall responses in vivo were not reduced. These data indicate that the nicotinic acid adenine dinucleotide phosphate/calcium signalling pathway is essential for the recruitment and the activation of autoaggressive effector T cells within their target organ. Interference with this signalling pathway suppresses the formation of autoimmune inflammatory lesions and thus might qualify as a novel strategy for the treatment of T cell mediated autoimmune diseases."],["dc.identifier.doi","10.1093/brain/awq135"],["dc.identifier.isi","000279473900008"],["dc.identifier.pmid","20519328"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19486"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Nicotinic acid adenine dinucleotide phosphate-mediated calcium signalling in effector T cells regulates autoimmunity of the central nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]