Lodygin, Dmitri

[["dc.bibliographiccitation.firstpage","46862"],["dc.bibliographiccitation.issue","30"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","46870"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Winter, Markus"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Verdoodt, Berlinda"],["dc.contributor.author","Hermeking, Heiko"],["dc.date.accessioned","2018-11-07T10:11:28Z"],["dc.date.available","2018-11-07T10:11:28Z"],["dc.date.issued","2016"],["dc.description.abstract","The p53-inducible cell cycle regulator 14-3-3 sigma exhibits tumor suppressive functions and is highly expressed in differentiating layers of the epidermis and hair follicles. 14-3-3 sigma/SFN/stratifin is frequently silenced in human epithelial cancers, and experimental down-regulation of 14-3-3 sigma expression immortalizes primary human keratinocytes. In the repeated-epilation (ER) mouse model, a heterozygous nonsense mutation of 14-3-3 sigma causes repeated hair-loss, hyper-proliferative epidermis, and spontaneous development of papillomas and squamous cell carcinomas in aging mice. Therefore, loss of 14-3-3 sigma function might contribute to epithelial tumor development. Here, we generated mice with loxP sites surrounding the single 14-3-3 sigma exon which allowed Cre-mediated deletion of the gene. 14-3-3 sigma-deficient mice are viable, but demonstrate a permanently disheveled fur. However, histological analyses of the skin did not reveal obvious defects in the hair follicles or the epidermis. Deletion of 14-3-3 sigma did not enhance spontaneous epidermal tumor development, whereas it increased the frequency and size of DMBA/TPA-induced papillomas. In conclusion, 14-3-3 sigma is dispensable for normal epidermal homeostasis but critical for suppression of chemically-induced skin carcinogenesis. In addition, these results suggest that the ER mutation of 14-3-3 sigma is not equivalent to loss of 14-3-3 sigma, but may represent a gain-of-function variant, which does not reflect the organismal function of wild-type 14-3-3 sigma."],["dc.identifier.doi","10.18632/oncotarget.10478"],["dc.identifier.isi","000385413000004"],["dc.identifier.pmid","27409835"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14135"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40051"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Deletion of 14-3-3 sigma sensitizes mice to DMBA/TPA-induced papillomatosis"],["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"]]

[["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.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger"],["dc.contributor.author","Kitz, Alexandra"],["dc.contributor.author","Nosov, Michail"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:02:16Z"],["dc.date.available","2018-11-07T09:02:16Z"],["dc.date.issued","2012"],["dc.identifier.isi","000312764800352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24643"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Boston, MA"],["dc.title","Direct imaging of T cell activation during experimental autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","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.firstpage","349"],["dc.bibliographiccitation.issue","7590"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","530"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","Krueger, Martin"],["dc.contributor.author","Vidoli, Stefano"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Mielke, Dorothee"],["dc.contributor.author","Brylla, Elke"],["dc.contributor.author","Issekutz, Thomas B."],["dc.contributor.author","Cabanas, Carlos"],["dc.contributor.author","Nelsons, Peter J."],["dc.contributor.author","Ziemssen, Tjalf"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Bechmann, Ingo"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T10:18:08Z"],["dc.date.available","2018-11-07T10:18:08Z"],["dc.date.issued","2016"],["dc.description.abstract","In multiple sclerosis, brain-reactive T cells invade the central nervous system (CNS) and induce a self-destructive inflammatory process. T-cell infiltrates are not only found within the parenchyma and the meninges, but also in the cerebrospinal fluid (CSF) that bathes the entire CNS tissue(1,2). How the T cells reach the CSF, their functionality, and whether they traffic between the CSF and other CNS compartments remains hypothetical(3-6). Here we show that effector T cells enter the CSF from the leptomeninges during Lewis rat experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. While moving through the three-dimensional leptomeningeal network of collagen fibres in a random Brownian walk, T cells were flushed from the surface by the flow of the CSF. The detached cells displayed significantly lower activation levels compared to T cells from the leptomeninges and CNS parenchyma. However, they did not represent a specialized non-pathogenic cellular sub-fraction, as their gene expression profile strongly resembled that of tissue-derived T cells and they fully retained their encephalitogenic potential. T-cell detachment from the leptomeninges was counteracted by integrins VLA-4 and LFA-1 binding to their respective ligands produced by resident macrophages. Chemokine signalling via CCR5/CXCR3 and antigenic stimulation of T cells in contact with the leptomeningeal macrophages enforced their adhesiveness. T cells floating in the CSF were able to reattach to the leptomeninges through steps reminiscent of vascular adhesion in CNS blood vessels, and invade the parenchyma. The molecular/cellular conditions for T-cell reattachment were the same as the requirements for detachment from the leptomeningeal milieu. Our data indicate that the leptomeninges represent a checkpoint at which activated T cells are licensed to enter the CNS parenchyma and non-activated T cells are preferentially released into the CSF, from where they can reach areas of antigen availability and tissue damage."],["dc.identifier.doi","10.1038/nature16939"],["dc.identifier.isi","000370327100040"],["dc.identifier.pmid","26863192"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41367"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1476-4687"],["dc.relation.issn","0028-0836"],["dc.title","Effector T-cell trafficking between the leptomeninges and the cerebrospinal fluid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","675"],["dc.bibliographiccitation.issue","7413"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.volume","488"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Sie, Christopher"],["dc.contributor.author","Streyl, Kristina"],["dc.contributor.author","Ulaganathan, Vijay Kumar"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Heckelsmiller, Klaus"],["dc.contributor.author","Nietfeld, Wilfried"],["dc.contributor.author","Ellwart, Joachim W."],["dc.contributor.author","Klinkert, Wolfgang E. F."],["dc.contributor.author","Lottaz, Claudio"],["dc.contributor.author","Nosov, Mikhail"],["dc.contributor.author","Brinkmann, Volker"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Lehrach, Hans"],["dc.contributor.author","Vingron, Martin"],["dc.contributor.author","Wekerle, Hartmut"],["dc.contributor.author","Fluegel-Koch, Cassandra"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:07:04Z"],["dc.date.available","2018-11-07T09:07:04Z"],["dc.date.issued","2012"],["dc.description.abstract","The blood-brain barrier (BBB) and the environment of the central nervous system (CNS) guard the nervous tissue from peripheral immune cells. In the autoimmune disease multiple sclerosis, myelin-reactive T-cell blasts are thought to transgress the BBB1,2 and create a pro-inflammatory environment in the CNS, thereby making possible a second autoimmune attack that starts from the leptomeningeal vessels and progresses into the parenchyma(3-6). Using a Lewis rat model of experimental autoimmune encephalomyelitis, we show here that contrary to the expectations of this concept, T-cell blasts do not efficiently enter the CNS and are not required to prepare the BBB for immune-cell recruitment. Instead, intravenously transferred T-cell blasts gain the capacity to enter the CNS after residing transiently within the lung tissues. Inside the lung tissues, they move along and within the airways to bronchus-associated lymphoid tissues and lung-draining mediastinal lymph nodes before they enter the blood circulation from where they reach the CNS. Effector T cells transferred directly into the airways showed a similar migratory pattern and retained their full pathogenicity. On their way the T cells fundamentally reprogrammed their gene-expression profile, characterized by downregulation of their activation program and upregulation of cellular locomotion molecules together with chemokine and adhesion receptors. The adhesion receptors include ninjurin 1, which participates in T-cell intravascular crawling on cerebral blood vessels. We detected that the lung constitutes a niche not only for activated T cells but also for resting myelin-reactive memory T cells. After local stimulation in the lung, these cells strongly proliferate and, after assuming migratory properties, enter the CNS and induce paralytic disease. The lung could therefore contribute to the activation of potentially autoaggressive T cells and their transition to a migratory mode as a prerequisite to entering their target tissues and inducing autoimmune disease."],["dc.identifier.doi","10.1038/nature11337"],["dc.identifier.isi","000308095100060"],["dc.identifier.pmid","22914092"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25704"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0028-0836"],["dc.title","T cells become licensed in the lung to enter the central nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:33:36Z"],["dc.date.available","2018-11-07T09:33:36Z"],["dc.date.issued","2014"],["dc.format.extent","204"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.548"],["dc.identifier.isi","000345192100537"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32001"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","In vivo visualization of the role of chemokines in migratory T cells during CNS inflammation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.artnumber","148721"],["dc.bibliographiccitation.journal","Biochimica et Biophysica Acta. Bioenergetics"],["dc.bibliographiccitation.volume","1863"],["dc.contributor.author","Shumanska, Magdalena"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Krause, Lena"],["dc.contributor.author","Ickes, Christian"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Dennerlein, Sven"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Bogeski, Ivan"],["dc.date.accessioned","2022-10-04T10:21:17Z"],["dc.date.available","2022-10-04T10:21:17Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/j.bbabio.2022.148721"],["dc.identifier.pii","S0005272822001918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114368"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.issn","0005-2728"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Differentiation-Induced Rearrangement of the Mitochondrial Calcium Uniporter Complex Regulates T-Cell-Mediated Immunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]