Kube, Dieter

[["dc.bibliographiccitation.firstpage","399"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","409"],["dc.bibliographiccitation.volume","230"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Wei, Wenbin"],["dc.contributor.author","Nagy, Eszter"],["dc.contributor.author","Prouzova, Zuzana"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Rowe, Martin"],["dc.contributor.author","Woodman, Ciaran B."],["dc.contributor.author","Murray, Paul G."],["dc.date.accessioned","2018-11-07T09:21:37Z"],["dc.date.available","2018-11-07T09:21:37Z"],["dc.date.issued","2013"],["dc.description.abstract","Hodgkin's lymphoma is unusual among B cell lymphomas, in so far as the malignant Hodgkin/Reed-Sternberg (HRS) cells lack a functional B cell receptor (BCR), as well as many of the required downstream signalling components. In Epstein-Barr virus (EBV)-positive cases of Hodgkin's lymphoma, HRS cells express the viral latent membrane proteins (LMP)-1 and -2A. LMP2A is thought to contribute to the pathogenesis of Hodgkin's lymphoma by providing a surrogate BCR-like survival signal. However, LMP2A has also been shown to induce the virus-replicative cycle in B cells, an event presumably incompatible with lymphomagenesis. In an attempt to resolve this apparent paradox, we compared the transcriptional changes observed in primary HRS cells with those induced by LMP2A and by BCR activation in primary human germinal centre (GC) B cells, the presumed progenitors of HRS cells. We found a subset of genes that were up-regulated by both LMP2A expression and BCR activation but which were down-regulated in primary HRS cells. These genes included EGR1, an immediate-early gene that is required for BCR-induced entry to the virus-replicative cycle. We present data supporting a model for the pathogenesis of EBV-positive Hodgkin's lymphoma in which LMP2A-expressing HRS cells lacking BCR signalling functions cannot induce EGR1 and are consequently protected from entry to the virus lytic cycle. The primary microarray data are available from GEO (http://www.ncbi.nlm.nih.gov/geo/) under series Accession No 46143. Copyright (c) 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.4198"],["dc.identifier.isi","000326160000007"],["dc.identifier.pmid","23592216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29152"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1096-9896"],["dc.relation.issn","0022-3417"],["dc.title","Suppression of the LMP2A target gene, EGR-1, protects Hodgkin's lymphoma cells from entry to the EBV lytic cycle"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","598"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","605"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Pinkert, D."],["dc.contributor.author","Smola-Hess, S."],["dc.contributor.author","Michels, A."],["dc.contributor.author","Ransohoff, Richard M."],["dc.contributor.author","Tesch, H."],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T11:07:44Z"],["dc.date.available","2018-11-07T11:07:44Z"],["dc.date.issued","2005"],["dc.description.abstract","The latent membrane protein 1 (LMP1) of Epstein-Barr Virus (EBV) is the main inducer of immuno-modulatory molecules affecting growth and survival of EBV-infected cells. However, the network of signalling pathways involved remains to be elucidated. Here we show that LMP1 may regulate cellular genes like IFN-gamma-inducible protein-10 kDa (IP-10) not only through transcriptional but also post-transcriptional mechanisms. LMP1-mediated IP-10 expression is independent from IFN-gamma, TNF-alpha or IL-18. Transcriptional activation of IP-10 by LMP1 or CD40 stimulation depends on an NF-KB motif within the proximal 435 bp fragment. Carboxy-terminal activating regions 1 or 2 of LMP1 are sufficient to direct IP-10 promoter activation. IP-10 induction is inhibited by blockade of p38/SAPK2 with SB 202190, which results in decreased IP-10 mRNA half-life without affecting IP-10 promoter activity. Thus, LMP1-mediated p38/SAPK2 activation regulates transcript stability. This new mechanism of gene regulation demonstrates the potential of the oncoprotein LMP1 to orchestrate a network of signalling pathways at different regulatory levels including mRNA stability. (C) 2004 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/ijc.20759"],["dc.identifier.isi","000227535400012"],["dc.identifier.pmid","15578697"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52637"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0020-7136"],["dc.title","The Epstein-Barr virus oncoprotein latent membrane protein 1 induces expression of the chemokine IP-10: Importance of mRNA half-life regulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","HAEMATOLOGICA-THE HEMATOLOGY JOURNAL"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Morgan, S. L."],["dc.contributor.author","Kuo, M."],["dc.contributor.author","Wei, W."],["dc.contributor.author","Chukwuma, M. B."],["dc.contributor.author","Arrand, John R."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Gordon, Jennifer"],["dc.contributor.author","Young, L. S."],["dc.contributor.author","Woodman, Ciaran B."],["dc.contributor.author","Murray, Paul G."],["dc.date.accessioned","2018-11-07T10:56:48Z"],["dc.date.available","2018-11-07T10:56:48Z"],["dc.date.issued","2007"],["dc.format.extent","41"],["dc.identifier.isi","000250470800107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50102"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ferrata Storti Foundation"],["dc.publisher.place","Pavia"],["dc.relation.conference","7th International Symposium on Hodgkin Lymphoma"],["dc.relation.eventlocation","Cologne, GERMANY"],["dc.relation.issn","0390-6078"],["dc.title","The EBV-encoded latent membrane protein-1 imposes on normal human germinal center B cells, a Hodgkin/Reed-Sternberg-like gene expression signature"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","593"],["dc.bibliographiccitation.issue","5709"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","596"],["dc.bibliographiccitation.volume","307"],["dc.contributor.author","Paludan, C."],["dc.contributor.author","Schmid, D."],["dc.contributor.author","Landthaler, M."],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Tuschl, T."],["dc.contributor.author","Münz, Christian"],["dc.date.accessioned","2018-11-07T08:31:51Z"],["dc.date.available","2018-11-07T08:31:51Z"],["dc.date.issued","2005"],["dc.description.abstract","CD4(+) T cells classically recognize antigens that are endocytosed and processed in lysosomes for presentation on major histocompatibility complex (MHC) class II molecules. Here, endogenous Epstein-Barr virus nuclear antigen 1 (EBNA1) was found to gain access to this pathway by autophagy. On inhibition of lysosomal acidification, EBNA1, the dominant CD4(+) T cell antigen of latent Epstein-Barr virus infection, slowly accumulated in cytosolic autophagosomes. In addition, inhibition of autophagy decreased recognition by EBNA1-specific CD4(+) T cell clones. Thus, lysosomal processing after autophagy may contribute to MHC class II-restricted surveillance of long-lived endogenous antigens including nuclear proteins relevant to disease."],["dc.identifier.doi","10.1126/science.1104904"],["dc.identifier.isi","000226694000051"],["dc.identifier.pmid","15591165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17213"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0036-8075"],["dc.title","Endogenous MHC class II processing of a viral nuclear antigen after autophagy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Bentink, Stefan"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Lenze, Dido"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Kuo, M."],["dc.contributor.author","Murray, P."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Vockerodt, Martina"],["dc.date.accessioned","2018-11-07T08:42:32Z"],["dc.date.available","2018-11-07T08:42:32Z"],["dc.date.issued","2010"],["dc.format.extent","107"],["dc.identifier.isi","000288603100400"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19723"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","21st Meeting of the European-Association-for-Cancer-Research"],["dc.relation.eventlocation","Oslo, NORWAY"],["dc.relation.issn","1359-6349"],["dc.title","A c-Myc induced gene expression signature in human germinal center B cells predicts subtypes of aggressive non-Hodgkin Lymphoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","459"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Genes and Immunity"],["dc.bibliographiccitation.lastpage","468"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Mormann, M."],["dc.contributor.author","Tomiuk, J."],["dc.contributor.author","Rieth, H."],["dc.contributor.author","Hua, Thanh-Duc"],["dc.contributor.author","Kremsner, P. G."],["dc.contributor.author","Vockerodt, Martina"],["dc.date.accessioned","2018-11-07T10:35:46Z"],["dc.date.available","2018-11-07T10:35:46Z"],["dc.date.issued","2003"],["dc.description.abstract","Different cytokine genotypes exist in the population, for example, as a result of selective pressure of infectious diseases. It may be that specific cytokine genotypes that are beneficial by creating a 'proinflammatory' phenotype predispose to severe inflammatory disease with worse clinical outcome. There is individual variation in the production of certain cytokines in relation to their genotypes. IL-10, IFN-gamma and TNF-alpha are key components in the regulation of immune responses and the balance of their expression levels is predictive in certain diseases. To describe cytokine genotypes, a one-tube PCR reaction was developed to analyse simultaneously DNA sequence variations of cytokine genes IL-10, IFN-gamma, and TNF. This multiplex PCR approach was used to provide genotypic data for two geographically independent donor groups from Germany and Gabon. Significant differences were obtained for the majority of sequence variations comparing both populations. However, the SNPs within the 5'-flanking region of the IL-10 gene at position -1087 and -6208 are comparable in their genic and genotypic behaviour. Comparing allelic and genotypic disequilibrium between pairs of loci revealed different association patterns for both populations according to the geographical polymorphism. This assay may improve immunogenetic studies in disease, characterized by disbalanced IL-10, IFN-gamma and TNF-alpha expression."],["dc.identifier.doi","10.1038/sj.gene.6364003"],["dc.identifier.isi","000185970500001"],["dc.identifier.pmid","14551598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45168"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1466-4879"],["dc.title","Simultaneous analysis of interleukin-10 gene microsatellites and single-nucleotide polymorphisms in parallel with tumour necrosis factor and interferon-gamma short tandem repeats by fluorescence-based polymerase chain reaction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","142"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","248"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Vrzalikova, Katerina"],["dc.contributor.author","Ibrahim, Maha"],["dc.contributor.author","Nagy, Eszter"],["dc.contributor.author","Margielewska, Sandra"],["dc.contributor.author","Hollows, Robert"],["dc.contributor.author","Lupino, Lauren"],["dc.contributor.author","Tooze, Reuben"],["dc.contributor.author","Care, Matthew"],["dc.contributor.author","Simmons, William"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Perry, Tracey"],["dc.contributor.author","Abdullah, Maizaton"],["dc.contributor.author","Foster, Stephen"],["dc.contributor.author","Reynolds, Gary"],["dc.contributor.author","Dowell, Alexander"],["dc.contributor.author","Rudzki, Zbigniew"],["dc.contributor.author","Krappmann, Daniel"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Woodman, Ciaran"],["dc.contributor.author","Wei, Wenbin"],["dc.contributor.author","Taylor, Graham"],["dc.contributor.author","Murray, Paul G"],["dc.date.accessioned","2020-12-10T14:07:02Z"],["dc.date.available","2020-12-10T14:07:02Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/path.5237"],["dc.identifier.eissn","1096-9896"],["dc.identifier.issn","0022-3417"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70111"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Regulation of S1PR2 by the EBV oncogene LMP1 in aggressive ABC‐subtype diffuse large B‐cell lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","640"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","British Journal of Haematology"],["dc.bibliographiccitation.lastpage","646"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Belge, G."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Irsch, J."],["dc.contributor.author","Siebert, Reiner"],["dc.contributor.author","Tesch, H."],["dc.contributor.author","Diehl, Volker"],["dc.contributor.author","Wolf, J."],["dc.contributor.author","Bullerdiek, J."],["dc.contributor.author","Staratschek-Jox, A."],["dc.date.accessioned","2018-11-07T09:43:49Z"],["dc.date.available","2018-11-07T09:43:49Z"],["dc.date.issued","2002"],["dc.description.abstract","In the vast majority of cases, Hodgkin - Reed Sternberg (H-RS) cells, the malignant cells in Hodgkin's lymphoma (HL), are derived from germinal centre B cells. In some cases, somatic mutations within the rearranged immunoglobulin heavy (IgH) chain genes were detected, rendering potentially functional gene rearrangements nonfunctional. In these H-RS cells the expression of high-affinity B-cell receptors (BCR) was prevented. As in other cases only one non-productive IgH chain gene rearrangement was amplified from H-RS cells, it was speculated whether, in these cases, the functionally rearranged IgH chain genes were lost. An alternative explanation might be that the rearranged genes could not be amplified owing to a high load of somatic mutations within the primer binding sites. Here, we showed that, in the HL-derived Epstein - Barr virus (EBV)-positive cell line L591, only one non-functional somatically mutated IgH gene rearrangement could be detected. The other potentially functional IgH gene rearrangement was lost as a result of an unbalanced translocation affecting the long arm of chromosome 14. Moreover, L591 cells express the EBV latent membrane proteins LMP1 and LMP2A, which might have contributed to the 'escape' of these cells from apoptosis within the germinal centre. We conclude that, apart from the introduction of 'crippling mutations' into the rearranged VDJ genes rearrangement, deletions of the IGH locus may be regarded as another mechanism to prevent the expression of a BCR in H-RS cells."],["dc.identifier.doi","10.1046/j.1365-2141.2002.03894.x"],["dc.identifier.isi","000179283600010"],["dc.identifier.pmid","12437638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34263"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0007-1048"],["dc.title","An unbalanced translocation involving chromosome 14 is the probable cause for loss of potentially functional rearranged immunoglobulin heavy chain genes in the Epstein-Barr virus-positive Hodgkin's lymphoma-derived cell line L591"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","936"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Leukemia"],["dc.bibliographiccitation.lastpage","944"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Holtick, U."],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Pinkert, D."],["dc.contributor.author","Schoof, Nils"],["dc.contributor.author","Sturzenhofecker, B."],["dc.contributor.author","Kussebi, N."],["dc.contributor.author","Lauber, Kirsten"],["dc.contributor.author","Wesselborg, S."],["dc.contributor.author","Loffler, D."],["dc.contributor.author","Horn, F."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T10:57:07Z"],["dc.date.available","2018-11-07T10:57:07Z"],["dc.date.issued","2005"],["dc.description.abstract","Classical Hodgkin lymphoma ( cHL) is a distinct malignancy of the immune system. Despite the progress made in the understanding of the biology of cHL, the transforming events remain to be elucidated. Recently, we demonstrated that the Janus kinase inhibitor AG490 blocked cellular proliferation and STAT3 phosphorylation in cHL. To explore the potential of constitutively activated STAT3 as a drug target and its role in cHL pathogenesis, different cHL cell lines were analyzed. Treatment of cHL cells by the protein tyrosine kinase inhibitor AG17 was associated with inhibition of cellular proliferation and cell cycle arrest. AG17 treatment was accompanied by decreased levels of STAT3 phosphorylation, whereas NF- kappa B and p38/ SAPK2 signaling were not inhibited. Incubation with AG17 or AG490 sensitized cHL cells to CD95/ Fas/ Apo- 1 or staurosporine-mediated apoptosis. Coincubation of tyrphostins with staurosporine was accompanied by rapid complete inhibition of STAT3 phosphorylation. RNA interference directed against STAT3 in L428 and L1236 cHL cells demonstrated that STAT3 is essential for cell proliferation of these cHL cells. In conclusion, these findings support the concept that STAT3 signaling is important in the pathogenesis of cHL and tyrphostins are agents for developing new therapeutic strategies."],["dc.identifier.doi","10.1038/sj.leu.2403750"],["dc.identifier.isi","000229323900009"],["dc.identifier.pmid","15912144"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50171"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0887-6924"],["dc.title","STAT3 is essential for Hodgkin lymphoma cell proliferation and is a target of tyrphostin AG17 which confers sensitization for apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5907"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","5917"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Vrzalikova, Katerina"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Leonard, Sarah"],["dc.contributor.author","Bell, Andrew I."],["dc.contributor.author","Wei, Wenbin"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Wright, Kenneth L."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Rowe, Martin"],["dc.contributor.author","Woodman, Ciaran B."],["dc.contributor.author","Murray, Paul G."],["dc.date.accessioned","2018-11-07T08:55:09Z"],["dc.date.available","2018-11-07T08:55:09Z"],["dc.date.issued","2011"],["dc.description.abstract","An important pathogenic event in Epstein-Barr virus (EBV)-associated lymphomas is the suppression of virus replication, which would otherwise lead to cell death. Because virus replication in B cells is intimately linked to their differentiation toward plasma cells, we asked whether the physiologic signals that drive normal B-cell differentiation are absent in EBV-transformed cells. We focused on BLIMP1 alpha, a transcription factor that is required for plasma cell differentiation and that is inactivated in diffuse large B-cell lymphomas. We show that BLIMP1 alpha expression is down-regulated after EBV infection of primary germinal center B cells and that the EBV oncogene, latent membrane protein-1 (LMP-1), is alone capable of inducing this down-regulation in these cells. Furthermore, the down-regulation of BLIMP1 alpha by LMP-1 was accompanied by a partial disruption of the BLIMP1 alpha transcriptional program, including the aberrant induction of MYC, the repression of which is required for terminal differentiation. Finally, we show that the ectopic expression of BLIMP1 alpha in EBV-transformed cells can induce the viral lytic cycle. Our results suggest that LMP-1 expression in progenitor germinal center B cells could contribute to the pathogenesis of EBV-associated lymphomas by down-regulating BLIMP1 alpha, in turn preventing plasma cell differentiation and induction of the viral lytic cycle. (Blood. 2011; 117(22): 5907-5917)"],["dc.identifier.doi","10.1182/blood-2010-09-307710"],["dc.identifier.isi","000291203200019"],["dc.identifier.pmid","21411757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22840"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.relation.issn","0006-4971"],["dc.title","Down-regulation of BLIMP1 alpha by the EBV oncogene, LMP-1, disrupts the plasma cell differentiation program and prevents viral replication in B cells: implications for the pathogenesis of EBV-associated B-cell lymphomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]