Kube, Dieter

[["dc.bibliographiccitation.volume","Förderkennzeichen BMBF 031A428B, Verbundnummer 01154498"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.editorcorporation","Universitätsmedizin Göttingen"],["dc.date.accessioned","2020-03-27T07:54:15Z"],["dc.date.available","2020-03-27T07:54:15Z"],["dc.date.issued","2019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/63374"],["dc.language.iso","de"],["dc.publisher","Universitätsmedizin Göttingen"],["dc.publisher.place","Göttingen"],["dc.title","Molekulare Mechanismen in Malignen Lymphomen - Demonstrator der personalisierten Medizin"],["dc.title.alternative","Vorhabensbezeichnung: Verbundprojekt: MMML-Demonstrators: Molekulare Mechanismen in Malignen Lymphomen - Demonstrator der personalisierten Medizin"],["dc.title.subtitle","Teil B / WP2, 4, 5, 6 : Schlussbericht : Laufzeit des Vorhabens: 01.03.2015-31.12.2018"],["dc.type","report"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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","2328"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","2338"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Tzvetkov, Mladen Vassilev"],["dc.contributor.author","Kreuz, Markus"],["dc.contributor.author","Ziepert, Marita"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T08:45:02Z"],["dc.date.available","2018-11-07T08:45:02Z"],["dc.date.issued","2010"],["dc.description.abstract","NAD(P)H oxidase is a major endogenous source of reactive oxygen species (ROS). ROS may not only be involved in carcinogenesis but also in efficacy of chemotherapeutic agents like doxorubicin. By a comprehensive genotyping approach covering 48 genetic polymorphisms (single-nucleotide polymorphisms) in five subunits of phagocytic NAD(P) H oxidase, we asked whether they affect gene expression, enzymatic activity, and outcome of CHO(E) P chemotherapy. A highly consistent effect was observed for the CYBA 640A>G variant. In peripheral blood granulocytes of 125 healthy volunteers, the G allele of 640A>G was associated with lower NAD(P) H oxidase activity (P = 0.006). Moreover, the G allele was associated with lower mRNA and protein expression (both P = 0.02). Of clinical importance, the outcome of patients suffering from non-Hodgkin lymphoma and treated with CHO(E) P regimen was dependent on the CYBA 640A>G polymorphism. In an exploratory study (n = 401), carriers of 640GG had an event-free survival (EFS) risk ratio of 1.95 [95% confidence interval (95% CI), 1.31-2.90; P = 0.001] compared with 640AA. In a confirmatory set (n = 477), the risk ratios were 1.53 (1.04-2.25, P = 0.03). The complete set of 878 patients showed a relative risk of 1.72 (1.30-2.26) and 1.59 (1.14-2.21) for EFS and overall survival, respectively. Further molecular-biological experiments showed lower expression and reduced stability of transcripts with the G allele in lymphoblastoid cell lines. Transfection of allele-specific plasmids into HEK293 cells elicited lower activity for the G allele in a luciferase reporter gene construct. Thus, CYBA 640A>G was shown to be a functional polymorphism with possible consequences for patients receiving CHO(E) P chemotherapy and might have further implications for other ROS-mediated modalities. Cancer Res; 70(6); 2328-38. (C) 2010 AACR."],["dc.identifier.doi","10.1158/0008-5472.CAN-09-2388"],["dc.identifier.isi","000278485900020"],["dc.identifier.pmid","20215507"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20334"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","0008-5472"],["dc.title","A Functional Polymorphism in the NAD(P)H Oxidase Subunit CYBA Is Related to Gene Expression, Enzyme Activity, and Outcome in Non-Hodgkin Lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","164"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Genes and Immunity"],["dc.bibliographiccitation.lastpage","167"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Hua, T-D"],["dc.contributor.author","Kloess, Marita"],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T11:04:26Z"],["dc.date.available","2018-11-07T11:04:26Z"],["dc.date.issued","2007"],["dc.description.abstract","The Interleukin 10 (IL-10) gene is highly polymorphic, and the IL-10_(1087AG) (rs1800896) gene variation is the only so far studied intensively in association with certain diseases. Conflicting data have been published about an association of IL-10_(1087AG) gene variation with lower rates of complete remission and lower overall survival (OS) in patients with diffuse large B-cell lymphoma. To further investigate this in malignant lymphoma, we established the IL-10 genotypes in patients from the NHL-B1/B2 studies from the German High-Grade Non-Hodgkin's Lymphoma Study Group. In our study, allele frequencies of lymphoma patients are comparable as in healthy controls. No increase of IL-10_(1087G) alleles was found. In addition we did not find any difference in OS or event-free survival between patients with IL-10_(1087AA) and the other genotypes. Comparable results were obtained for the IL-10 loci at -3538 (A/T), -1354 (A/G), -824 (C/T) and -597 (A/C) (rs1800890, rs1800893, rs1800871 and rs1800872)."],["dc.identifier.doi","10.1038/sj.gene.6364364"],["dc.identifier.isi","000244715500010"],["dc.identifier.pmid","17215862"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51844"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1466-4879"],["dc.title","The interleukin-10 gene promoter polymorphism - 1087AG does not correlate with clinical outcome in non-Hodgkin's lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","515"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","525"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Knoell, Ralph"],["dc.contributor.author","Postel, Ruben"],["dc.contributor.author","Wang, Jianming"],["dc.contributor.author","Kraetzner, Ralph"],["dc.contributor.author","Hennecke, Gerrit"],["dc.contributor.author","Vacaru, Andrei M."],["dc.contributor.author","Vakeel, Padmanabhan"],["dc.contributor.author","Schubert, Cornelia"],["dc.contributor.author","Murthy, Kenton"],["dc.contributor.author","Rana, Brinda K."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Knoell, Gudrun"],["dc.contributor.author","Schaefer, Katrin"],["dc.contributor.author","Hayashi, Takeharu"],["dc.contributor.author","Holm, Torbjorn"],["dc.contributor.author","Kimura, Akinori"],["dc.contributor.author","Schork, Nicholas"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Schultheiss, Heinz-Peter"],["dc.contributor.author","Schaper, Wolfgang"],["dc.contributor.author","Schaper, Jutta"],["dc.contributor.author","Bos, Erik"],["dc.contributor.author","Hertog, Jeroen den"],["dc.contributor.author","van Eeden, Fredericus J. M."],["dc.contributor.author","Peters, Peter J."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Chien, Kenneth R."],["dc.contributor.author","Bakkers, Jeroen"],["dc.date.accessioned","2017-09-07T11:49:27Z"],["dc.date.available","2017-09-07T11:49:27Z"],["dc.date.issued","2007"],["dc.description.abstract","Background - Extracellular matrix proteins, such as laminins, and endothelial cells are known to influence cardiomyocyte performance; however, the underlying molecular mechanisms remain poorly understood. Methods and Results - We used a forward genetic screen in zebrafish to identify novel genes required for myocardial function and were able to identify the lost-contact (loc) mutant, which encodes a nonsense mutation in the integrin-linked kinase ( ilk) gene. This loc/ilk mutant is associated with a severe defect in cardiomyocytes and endothelial cells that leads to severe myocardial dysfunction. Additional experiments revealed the epistatic regulation between laminin-alpha 4 (Lama4), integrin, and Ilk, which led us to screen for mutations in the human ILK and LAMA4 genes in patients with severe dilated cardiomyopathy. We identified 2 novel amino acid residue - altering mutations (2828C > T [Pro943Leu] and 3217C > T [Arg1073X]) in the integrin-interacting domain of the LAMA4 gene and 1 mutation (785C > T [Ala262Val]) in the ILK gene. Biacore quantitative protein/protein interaction data, which have been used to determine the equilibrium dissociation constants, point to the loss of integrin-binding capacity in case of the Pro943Leu (K-d = 5 +/- 3 mu mol/L) and Arg1073X LAMA4 (K-d=1 +/- 0.2 mu mol/L) mutants compared with the wild-type LAMA4 protein (K-d=440 +/- 20nmol/L). Additional functional data point to the loss of endothelial cells in affected patients as a direct consequence of the mutant genes, which ultimately leads to heart failure. Conclusions - This is the first report on mutations in the laminin, integrin, and ILK system in human cardiomyopathy, which has consequences for endothelial cells as well as for cardiomyocytes, thus providing a new genetic basis for dilated cardiomyopathy in humans."],["dc.identifier.doi","10.1161/CIRCULATIONAHA.107.689984"],["dc.identifier.gro","3143464"],["dc.identifier.isi","000248456000009"],["dc.identifier.pmid","17646580"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/981"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0009-7322"],["dc.title","Laminin-alpha 4 and integrin-linked kinase mutations cause human cardiomyopathy via simultaneous defects in cardiomyocytes and endothelial cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1147"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","1158"],["dc.bibliographiccitation.volume","140"],["dc.contributor.author","Feist, Maren"],["dc.contributor.author","Kemper, Judith"],["dc.contributor.author","Taruttis, Franziska"],["dc.contributor.author","Rehberg, Thorsten"],["dc.contributor.author","Engelmann, Julia C."],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T10:27:05Z"],["dc.date.available","2018-11-07T10:27:05Z"],["dc.date.issued","2017"],["dc.description.abstract","A network of autocrine and paracrine signals defines B cell homeostasis and is thought to be involved in transformation processes. Investigating interactions of these microenvironmental factors and their relation to proto-oncogenes as c-Myc (MYC) is fundamental to understand the biology of B cell lymphoma. Therefore, B cells with conditional MYC expression were stimulated with CD40L, insulin-like growth factor 1, alpha-IgM, Interleukin-10 (IL10) and CpG alone or in combination. The impact of forty different interventions on cell proliferation was investigated in MYC deprived cells and calculated by linear regression. Combination of CpG and IL10 led to a strong synergistic activation of cell proliferation (S-phase/doubling of total cell number) comparable to cells with high MYC expression. A synergistic up-regulation of CDK4, CDK6 and CCND3 expression by IL10 and CpG treatment was causal for this proliferative effect as shown by qRT-PCR analysis and inhibition of the CDK4/6 complex by PD0332991. Furthermore, treatment of stimulated MYC deprived cells with MLN120b, ACHP, Pyridone 6 or Ruxolitinib showed that IL10/CpG induced proliferation and CDK4 expression were JAK/STAT3 and IKK/NF-jB dependent. This was further supported by STAT3 and p65/RELA knockdown experiments, showing strongest effects on cell proliferation and CDK4 expression after double knockdown. Additionally, chromatin immunoprecipitation revealed a dual binding of STAT3 and p65 to the proximal promotor of CDK4 after IL10/CpG treatment. Therefore, the observed synergism of IL10R and TLR9 signalling was able to induce proliferation in a comparable way as aberrant MYC and might play a role in B cell homeostasis or transformation."],["dc.description.sponsorship","BMBF network eBio \"MMML-MycSys\" [BMBF-FKZ 0316166E, 0316166G, 0316166F]"],["dc.identifier.doi","10.1002/ijc.30444"],["dc.identifier.isi","000393976100017"],["dc.identifier.pmid","27668411"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43179"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","Synergy of interleukin 10 and toll-like receptor 9 signalling in B cell proliferation: Implications for lymphoma pathogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","British Journal of Haematology"],["dc.bibliographiccitation.volume","159"],["dc.contributor.author","Richter, J."],["dc.contributor.author","Schlesner, Matthias"],["dc.contributor.author","Leich, Ellen"],["dc.contributor.author","Burkhardt, Birgit"],["dc.contributor.author","Hoffmann, S."],["dc.contributor.author","Szczepanowski, Monika"],["dc.contributor.author","Kreuz, Markus"],["dc.contributor.author","Lenze, Dido"],["dc.contributor.author","Bernhart, S."],["dc.contributor.author","Rosolowski, Maciej"],["dc.contributor.author","Hoell, Jessica I."],["dc.contributor.author","Lawerenz, Chris"],["dc.contributor.author","Jaeger, Nadine"],["dc.contributor.author","Hutter, Barbara"],["dc.contributor.author","Langerberger, D."],["dc.contributor.author","Ammerpohl, Ole"],["dc.contributor.author","Binder, H."],["dc.contributor.author","Borkhardt, Arndt"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Claviez, Alexander"],["dc.contributor.author","Pischimarov, Jordan"],["dc.contributor.author","Dreyling, M."],["dc.contributor.author","Eils, Roland"],["dc.contributor.author","Hansmann, M-L"],["dc.contributor.author","Binder, V."],["dc.contributor.author","Hornig, Nadine"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Korbel, Jan O."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Kueppers, Ralf"],["dc.contributor.author","Lichter, Peter"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Moeller, Peter"],["dc.contributor.author","Pott, C."],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Schreiber, Sefan"],["dc.contributor.author","Schilhabel, Markus"],["dc.contributor.author","Scholtysik, Rene"],["dc.contributor.author","Stadler, Peter F."],["dc.contributor.author","Trautmann, Heiko"],["dc.contributor.author","Wagener, R."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Rosenstiel, Philip"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Siebert, Reiner"],["dc.date.accessioned","2018-11-07T09:03:43Z"],["dc.date.available","2018-11-07T09:03:43Z"],["dc.date.issued","2012"],["dc.format.extent","7"],["dc.identifier.isi","000312889800013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24954"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","4th International Symposium on Childhood, Adolescent and Young Adult Non-Hodgkins Lymphoma"],["dc.relation.eventlocation","New York, NY"],["dc.relation.issn","0007-1048"],["dc.title","Sequencing of pediatric Burkitt lymphoma within the ICGC MMML-Seq project"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Haematologica"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Freytag, N."],["dc.contributor.author","Pommerenke, Claudia"],["dc.contributor.author","Merkhoffer, Y."],["dc.contributor.author","Arranz, J. Arribas"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Drexler, Hans G."],["dc.contributor.author","Quentmeier, Hilmar"],["dc.contributor.author","Eberth, Sonja"],["dc.date.accessioned","2018-11-07T10:22:34Z"],["dc.date.available","2018-11-07T10:22:34Z"],["dc.date.issued","2017"],["dc.format.extent","569"],["dc.identifier.isi","000404127004206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42301"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Ferrata Storti Foundation"],["dc.publisher.place","Pavia"],["dc.relation.conference","22nd Congress of the European-Hematology-Association"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","0390-6078"],["dc.title","HIGH EXPRESSION LEVELS OF MIR23A CLUSTER IN DLBCL ANTAGONIZE INDUCTION OF APOPTOSIS"],["dc.type","conference_abstract"],["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","Schoof, Nils"],["dc.contributor.author","von Bonin, E."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T10:56:54Z"],["dc.date.available","2018-11-07T10:56:54Z"],["dc.date.issued","2007"],["dc.format.extent","42"],["dc.identifier.isi","000250470800112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50124"],["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","Janus kinases are targets of tyrphostin AG17 and HSP90-inhibitor 17-AAG in classical 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","53"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","BioTechniques"],["dc.bibliographiccitation.lastpage","61"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Taruttis, Franziska"],["dc.contributor.author","Feist, Maren"],["dc.contributor.author","Schwarzfischer, Phillip"],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Engelmann, Julia C."],["dc.date.accessioned","2018-11-07T10:27:58Z"],["dc.date.available","2018-11-07T10:27:58Z"],["dc.date.issued","2017"],["dc.description.abstract","Gene expression measurements are typically performed on a fixed-weight aliquot of RNA, which assumes that the total number of transcripts per cell stays nearly constant across all conditions. In cases where this assumption does not hold (e.g., when comparing cell types with different cell sizes) the expression data provide a distorted view of cellular events. Assuming constant numbers of total transcripts, increases in expression of some RNAs must be compensated for by decreases in expression of others. Therefore, we propose calibrating gene expression data to an external reference point, the number of cells in the sample, using whole-cell spike-ins. In a systematic dilution experiment, we mixed varying numbers of human cells with fixed numbers of Drosophila melanogaster cells and scaled the expression levels of the human genes relative to those of the Drosophila genes. This approach restored the original gene expression ratios generated by the dilutions. We then used Drosophila whole-cell spike-ins to uncover non-symmetric gene expression changes, in this case much larger numbers of induced than repressed genes, under perturbations of the human cell line P493-6. Drosophila whole-cell spike-ins are an experimentally and computationally easy and low-priced method to derive mRNA fold changes of absolute abundances from RNA sequencing (RNA-Seq) and quantitative real-time PCR (qPCR) data."],["dc.identifier.doi","10.2144/000114514"],["dc.identifier.isi","000393884800003"],["dc.identifier.pmid","28193148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43328"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biotechniques Office"],["dc.relation.issn","1940-9818"],["dc.relation.issn","0736-6205"],["dc.title","External calibration with Drosophila whole-cell spike-ins delivers absolute mRNA fold changes from human RNA-Seq and qPCR data"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]