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2. Supplementary Table 9 from Hypoxia Modulates EWS-FLI1 Transcriptional Signature and Enhances the Malignant Properties of Ewing's Sarcoma Cells In vitro

Author

Aryee, Dave N.T., primary, Niedan, Stephan, primary, Kauer, Maximilian, primary, Schwentner, Raphaela, primary, Bennani-Baiti, Idriss M., primary, Ban, Jozef, primary, Muehlbacher, Karin, primary, Kreppel, Michael, primary, Walker, Robert L., primary, Meltzer, Paul, primary, Poremba, Christopher, primary, Kofler, Reinhard, primary, and Kovar, Heinrich, primary

Published
2023
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3. Supplementary Tables 1-6 from Hypoxia Modulates EWS-FLI1 Transcriptional Signature and Enhances the Malignant Properties of Ewing's Sarcoma Cells In vitro

Author

Aryee, Dave N.T., primary, Niedan, Stephan, primary, Kauer, Maximilian, primary, Schwentner, Raphaela, primary, Bennani-Baiti, Idriss M., primary, Ban, Jozef, primary, Muehlbacher, Karin, primary, Kreppel, Michael, primary, Walker, Robert L., primary, Meltzer, Paul, primary, Poremba, Christopher, primary, Kofler, Reinhard, primary, and Kovar, Heinrich, primary

Published
2023
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4. Supplementary Table 7 from Hypoxia Modulates EWS-FLI1 Transcriptional Signature and Enhances the Malignant Properties of Ewing's Sarcoma Cells In vitro

Author

Aryee, Dave N.T., primary, Niedan, Stephan, primary, Kauer, Maximilian, primary, Schwentner, Raphaela, primary, Bennani-Baiti, Idriss M., primary, Ban, Jozef, primary, Muehlbacher, Karin, primary, Kreppel, Michael, primary, Walker, Robert L., primary, Meltzer, Paul, primary, Poremba, Christopher, primary, Kofler, Reinhard, primary, and Kovar, Heinrich, primary

Published
2023
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5. Supplementary Figure 1 from Hypoxia Modulates EWS-FLI1 Transcriptional Signature and Enhances the Malignant Properties of Ewing's Sarcoma Cells In vitro

Author

Aryee, Dave N.T., primary, Niedan, Stephan, primary, Kauer, Maximilian, primary, Schwentner, Raphaela, primary, Bennani-Baiti, Idriss M., primary, Ban, Jozef, primary, Muehlbacher, Karin, primary, Kreppel, Michael, primary, Walker, Robert L., primary, Meltzer, Paul, primary, Poremba, Christopher, primary, Kofler, Reinhard, primary, and Kovar, Heinrich, primary

Published
2023
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6. Data from Hypoxia Modulates EWS-FLI1 Transcriptional Signature and Enhances the Malignant Properties of Ewing's Sarcoma Cells In vitro

Author

Aryee, Dave N.T., primary, Niedan, Stephan, primary, Kauer, Maximilian, primary, Schwentner, Raphaela, primary, Bennani-Baiti, Idriss M., primary, Ban, Jozef, primary, Muehlbacher, Karin, primary, Kreppel, Michael, primary, Walker, Robert L., primary, Meltzer, Paul, primary, Poremba, Christopher, primary, Kofler, Reinhard, primary, and Kovar, Heinrich, primary

Published
2023
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7. Supplementary Figure Legend 1, Table Legends 1-6 from Hypoxia Modulates EWS-FLI1 Transcriptional Signature and Enhances the Malignant Properties of Ewing's Sarcoma Cells In vitro

Author

Aryee, Dave N.T., primary, Niedan, Stephan, primary, Kauer, Maximilian, primary, Schwentner, Raphaela, primary, Bennani-Baiti, Idriss M., primary, Ban, Jozef, primary, Muehlbacher, Karin, primary, Kreppel, Michael, primary, Walker, Robert L., primary, Meltzer, Paul, primary, Poremba, Christopher, primary, Kofler, Reinhard, primary, and Kovar, Heinrich, primary

Published
2023
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8. Supplementary Table 8b from Hypoxia Modulates EWS-FLI1 Transcriptional Signature and Enhances the Malignant Properties of Ewing's Sarcoma Cells In vitro

Author

Aryee, Dave N.T., primary, Niedan, Stephan, primary, Kauer, Maximilian, primary, Schwentner, Raphaela, primary, Bennani-Baiti, Idriss M., primary, Ban, Jozef, primary, Muehlbacher, Karin, primary, Kreppel, Michael, primary, Walker, Robert L., primary, Meltzer, Paul, primary, Poremba, Christopher, primary, Kofler, Reinhard, primary, and Kovar, Heinrich, primary

Published
2023
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10. ETV6/RUNX1-positive relapses evolve from an ancestral clone and frequently acquire deletions of genes implicated in glucocorticoid signaling

Author

Kuster, Lilian, Grausenburger, Reinhard, Fuka, Gerhard, Kaindl, Ulrike, Krapf, Gerd, Inthal, Andrea, Mann, Georg, Kauer, Maximilian, Rainer, Johannes, Kofler, Reinhard, Hall, Andrew, Metzler, Markus, Meyer, Lüder Hinrich, Meyer, Claus, Harbott, Jochen, Marschalek, Rolf, Strehl, Sabine, Haas, Oskar A., and Panzer-Grümayer, Renate

Published
2011
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11. Quantitative proteomic analysis reveals maturation as a mechanism underlying glucocorticoid resistance in B lineage ALL and re-sensitization by JNK inhibition

Author

Nicholson, Lindsay, Evans, Caroline A., Matheson, Elizabeth, Minto, Lynne, Keilty, Christopher, Sanichar, Maryna, Case, Marian, Schwab, Claire, Williamson, Daniel, Rainer, Johannes, Harrison, Christine J., Kofler, Reinhard, Hall, Andrew G., Redfern, Christopher P. F., Whetton, Anthony D., and Irving, Julie A. E.

Published
2015
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13. LAMTOR/Ragulator regulates lipid metabolism in macrophages and foam cell differentiation

Author

Lamberti, Giorgia, De Smet, Cedric H., Angelova, Mihaela, Kremser, Leopold, Taub, Nicole, Herrmann, Caroline, Hess, Michael W., Rainer, Johannes, Tancevski, Ivan, Schweigreiter, Rüdiger, Kofler, Reinhard, Schmiedinger, Thomas, Vietor, Ilja, Trajanoski, Zlatko, Ejsing, Christer S., Lindner, Herbert H., Huber, Lukas A., and Stasyk, Taras

Subjects
Macrophages, organelle proteomics, Proteins, Cell Differentiation, Lipid Droplets, Lipid Metabolism, Cell Fate Determination, Research Letters, foam cells, macrophages, transcriptomics, Mice, Research Letter, LAMTOR, Animals, Cholesterol Esters, ragulator, Transcriptome, Cells, Cultured
Abstract

Late endosomal/lysosomal adaptor and MAPK and mTOR activator (LAMTOR/Ragulator) is a scaffold protein complex that anchors and regulates multiprotein signaling units on late endosomes/lysosomes. To identify LAMTOR-modulated endolysosomal proteins, primary macrophages were derived from bone marrow of conditional knockout mice carrying a specific deletion of LAMTOR2 in the monocyte/macrophage cell lineage. Affymetrix-based transcriptomic analysis and quantitative iTRAQ-based organelle proteomic analysis of endosomes derived from macrophages were performed. Further analyses showed that LAMTOR could be a novel regulator of foam cell differentiation. The lipid droplet formation phenotype observed in macrophages was additionally confirmed in MEFs, where lipidomic analysis identified cholesterol esters as specifically downregulated in LAMTOR2 knockout cells. The data obtained indicate a function of LAMTOR2 in lipid metabolism.

Published
2019

14. CLP1 links tRNA metabolism to progressive motor-neuron loss

Author

Hanada, Toshikatsu, Weitzer, Stefan, Mair, Barbara, Bernreuther, Christian, Wainger, Brian J., Ichida, Justin, Hanada, Reiko, Orthofer, Michael, Cronin, Shane J., Komnenovic, Vukoslav, Minis, Adi, Sato, Fuminori, Mimata, Hiromitsu, Yoshimura, Akihiko, Tamir, Ido, Rainer, Johannes, Kofler, Reinhard, Yaron, Avraham, Eggan, Kevin C., Woolf, Clifford J., Glatze, Markus, Herbst, Ruth, Martinez, Javier, and Penninger, Josef M.

Subjects
Neuromuscular diseases -- Research, Motor neurons -- Observations, Phosphotransferases -- Properties, Transfer RNA -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

CLP1 was the first mammalian RNA kinase to be identified. However, determining its in vivo function has been elusive. Here we generated kinase-dead Clpl ([Clp1.sup.K/K]) mice that show a progressive loss of spinal motor neurons associated with axonal degeneration in the peripheral nerves and denervation of neuromuscular junctions, resulting in impaired motor function, muscle weakness, paralysis and fatal respiratory failure. Transgenic rescue experiments show that CLP1 functions in motor neurons. Mechanistically, loss of CLP1 activity results in accumulation of a novel set of small RNA fragments, derived from aberrant processing of tyrosine pre-transfer RNA. These tRNA fragments sensitize cells to oxidative-stress-induced p53 (also known as TRP53) activation and p53-dependent cell death. Genetic inactivation of p53 rescues [Clp1.sup.K/K] mice from the motor neuron loss, muscle denervation and respiratory failure. Our experiments uncover a mechanistic link between tRNA processing, formation of a new RNA species and progressive loss of lower motor neurons regulated by p53., RNA molecules undergo co- and post-transcriptional processing, leading to mature, functional RNAs. In mammals and archaea CLP1 proteins are kinases that phosphorylate the 5' hydroxyl ends of RNA (1-3). Human [...]

Published
2013
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22. Analysis of common glucocorticoid response genes in childhood acute lymphoblastic leukemia in vivo identifies cell cycle but not apoptosis genes

Author

Aneichyk, Tatsiana, primary, Schmidt, Stefan, additional, Bindreither, Daniel, additional, Kroesbacher, Armin, additional, Mueller, Nikola S, additional, Meister, Bernhard, additional, Crazzolara, Roman, additional, Mann, Georg, additional, Panzer-Gruemayer, Renate, additional, Kofler, Reinhard, additional, Rainer, Johannes, additional, and Geley, Stephan, additional

Published
2020
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32. Expression, regulation and function of phosphofructo-kinase/fructose-biphosphatases (PFKFBs) in glucocorticoid-induced apoptosis of acute lymphoblastic leukemia cells

Author

Schmidt Stefan, Rainer Johannes, Janjetovic Kristina, Carlet Michela, Panzer-Grümayer Renate, Mann Georg, Prelog Martina, Meister Bernhard, Ploner Christian, and Kofler Reinhard

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Glucocorticoids (GCs) cause apoptosis and cell cycle arrest in lymphoid cells and constitute a central component in the therapy of lymphoid malignancies, most notably childhood acute lymphoblastic leukemia (ALL). PFKFB2 (6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-2), a kinase controlling glucose metabolism, was identified by us previously as a GC response gene in expression profiling analyses performed in children with ALL during initial systemic GC mono-therapy. Since deregulation of glucose metabolism has been implicated in apoptosis induction, this gene and its relatives, PFKFB1, 3, and 4, were further analyzed. Methods Gene expression analyses of isolated lymphoblasts were performed on Affymetrix HGU133 Plus 2.0 microarrays. GCRMA normalized microarray data were analyzed using R-Bioconductor packages version 2.5. Functional gene analyses of PFKFB2-15A and -15B isoforms were performed by conditional gene over-expression experiments in the GC-sensitive T-ALL model CCRF-CEM. Results Expression analyses in additional ALL children, non-leukemic individuals and leukemic cell lines confirmed frequent PFKFB2 induction by GC in most systems sensitive to GC-induced apoptosis, particularly T-ALL cells. The 3 other family members, in contrast, were either absent or only weakly expressed (PFKFB1 and 4) or not induced by GC (PFKFB3). Conditional PFKFB2 over-expression in the CCRF-CEM T-ALL in vitro model revealed that its 2 splice variants (PFKFB2-15A and PFKFB2-15B) had no detectable effect on cell survival. Moreover, neither PFKFB2 splice variant significantly affected sensitivity to, or kinetics of, GC-induced apoptosis. Conclusions Our data suggest that, at least in the model system investigated, PFKFB2 is not an essential upstream regulator of the anti-leukemic effects of GC.

Published
2010
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35. LAMTOR/Ragulator regulates lipid metabolism in macrophages and foam cell differentiation.

Author

Lamberti, Giorgia, De Smet, Cedric H., Angelova, Mihaela, Kremser, Leopold, Taub, Nicole, Herrmann, Caroline, Hess, Michael W., Rainer, Johannes, Tancevski, Ivan, Schweigreiter, Rüdiger, Kofler, Reinhard, Schmiedinger, Thomas, Vietor, Ilja, Trajanoski, Zlatko, Ejsing, Christer S., Lindner, Herbert H., Huber, Lukas A., and Stasyk, Taras

Subjects
LIPID metabolism, CELL differentiation, LYSOSOMES, FOAM cells, BONE marrow, SCAFFOLD proteins
Abstract

Late endosomal/lysosomal adaptor and MAPK and mTOR activator (LAMTOR/Ragulator) is a scaffold protein complex that anchors and regulates multiprotein signaling units on late endosomes/lysosomes. To identify LAMTOR‐modulated endolysosomal proteins, primary macrophages were derived from bone marrow of conditional knockout mice carrying a specific deletion of LAMTOR2 in the monocyte/macrophage cell lineage. Affymetrix‐based transcriptomic analysis and quantitative iTRAQ‐based organelle proteomic analysis of endosomes derived from macrophages were performed. Further analyses showed that LAMTOR could be a novel regulator of foam cell differentiation. The lipid droplet formation phenotype observed in macrophages was additionally confirmed in MEFs, where lipidomic analysis identified cholesterol esters as specifically downregulated in LAMTOR2 knockout cells. The data obtained indicate a function of LAMTOR2 in lipid metabolism. [ABSTRACT FROM AUTHOR]

Published
2020
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36. 3D-cultivation of NSCLC cell lines induce gene expression alterations of key cancer-associated pathways and mimicin-vivoconditions

Author

Gamerith, Gabriele, primary, Rainer, Johannes, additional, Huber, Julia M., additional, Hackl, Hubert, additional, Trajanoski, Zlatko, additional, Koeck, Stefan, additional, Lorenz, Edith, additional, Kern, Johann, additional, Kofler, Reinhard, additional, Kelm, Jens M., additional, Zwierzina, Heinz, additional, and Amann, Arno, additional

Published
2017
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37. Translational profiling in childhood acute lymphoblastic leukemia: no evidence for glucocorticoid regulation of mRNA translation

Author

Aneichyk, Tatsiana, Bindreither, Daniel, Mantinger, Christine, Grazio, Daniela, Goetsch, Katrin, Kofler, Reinhard, and Rainer, Johannes

Subjects
Genome, Human, Gene Expression Profiling, Polysome profiling, Acute lymphoblastic leukemia, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Translatome, Gene regulation, Cell Line, Tumor, Protein Biosynthesis, Genetics, Humans, RNA, Messenger, Transcriptome, Glucocorticoids, Biotechnology, Research Article, Oligonucleotide Array Sequence Analysis
Abstract

Background Glucocorticoids (GCs) are natural stress induced steroid hormones causing cell cycle arrest and cell death in lymphoid tissues. Therefore they are the central component in the treatment of lymphoid malignancies, in particular childhood acute lymphoblastic leukemia (chALL). GCs act mainly via regulating gene transcription, which has been intensively studied by us and others. GC control of mRNA translation has also been reported but has never been assessed systematically. In this study we investigate the effect of GCs on mRNA translation on a genome-wide scale. Results Childhood T- (CCRF-CEM) and precursor B-ALL (NALM6) cells were exposed to GCs and subjected to “translational profiling”, a technique combining sucrose-gradient fractionation followed by Affymetrix Exon microarray analysis of mRNA from different fractions, to assess the translational efficiency of the expressed genes. Analysis of GC regulation in ribosome-bound fractions versus transcriptional regulation revealed no significant differences, i.e., GC did not entail a significant shift between ribosomal bound and unbound mRNAs. Conclusions In the present study we analyzed for the first time possible effects of GC on the translational efficiency of expressed genes in two chALL model systems employing whole genome polysome profiling. Our results did not reveal significant differences in translational efficiency of expressed genes thereby arguing against a potential widespread regulatory effect of GCs on translation at least in the investigated in vitro systems. Electronic supplementary material The online version of this article (doi:10.1186/1471-2164-14-844) contains supplementary material, which is available to authorized users.

Published
2013

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