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5. High levels of onco-miR-21 contribute to the senescence-induced growth arrest in normal human cells and its knock-down increases the replicative lifespan

Author

Dellago, Hanna, Preschitz-Kammerhofer, Barbara, Terlecki-Zaniewicz, Lucia, Schreiner, Carina, Fortschegger, Klaus, Chang, Martina W.-F., Hackl, Matthias, Monteforte, Rossella, Kühnel, Harald, Schosserer, Markus, Gruber, Florian, Tschachler, Erwin, Scheideler, Marcel, Grillari-Voglauer, Regina, Grillari, Johannes, and Wieser, Matthias

Published
2015
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7. High levels of oncomiR-21 contribute to the senescence-induced growth arrest in normal human cells and its knock-down increases the replicative lifespan

Author

Dellago, Hanna, Preschitz-Kammerhofer, Barbara, Terlecki-Zaniewicz, Lucia, Schreiner, Carina, Fortschegger, Klaus, Chang, Martina W.-F., Hackl, Matthias, Monteforte, Rossella, Kühnel, Harald, Schosserer, Markus, Gruber, Florian, Tschachler, Erwin, Scheideler, Marcel, Grillari-Voglauer, Regina, Grillari, Johannes, and Wieser, Matthias

Published
2013
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8. miR-17, miR-19b, miR-20a, and miR-106a are down-regulated in human aging

Author

Hackl, Matthias, Brunner, Stefan, Fortschegger, Klaus, Schreiner, Carina, Micutkova, Lucia, Mück, Christoph, Laschober, Gerhard T., Lepperdinger, Günter, Sampson, Natalie, Berger, Peter, Herndler-Brandstetter, Dietmar, Wieser, Matthias, Kühnel, Harald, Strasser, Alois, Rinnerthaler, Mark, Breitenbach, Michael, Mildner, Michael, Eckhart, Leopold, Tschachler, Erwin, Trost, Andrea, Bauer, Johann W., Papak, Christine, Trajanoski, Zlatko, Scheideler, Marcel, Grillari-Voglauer, Regina, Grubeck-Loebenstein, Beatrix, Jansen-Dürr, Pidder, and Grillari, Johannes

Published
2010
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11. CD371 cell surface expression: a unique feature of DUX4-rearranged acute lymphoblastic leukemia

Author

Schinnerl, Dagmar, Mejstrikova, Ester, Schumich, Angela, Zaliova, Marketa, Fortschegger, Klaus, Nebral, Karin, Attarbaschi, Andishe, Fiser, Karel, Kauer, Maximilian O, Popitsch, Niko, Haslinger, Sabrina, Inthal, Andrea, Buldini, Barbara, Basso, Giuseppe, Bourquin, Jean-Pierre, Gaipa, Giuseppe, Brüggemann, Monika, Feuerstein, Tamar, Maurer-Granofszky, Margarita, Panzer-Grümayer, Renate, Trka, Jan, Mann, Georg, Haas, Oskar A, Hrusak, Ondrej, Dworzak, Michael N, Strehl, Sabine, Schinnerl, Dagmar, Mejstrikova, Ester, Schumich, Angela, Zaliova, Marketa, Fortschegger, Klaus, Nebral, Karin, Attarbaschi, Andishe, Fiser, Karel, Kauer, Maximilian O, Popitsch, Niko, Haslinger, Sabrina, Inthal, Andrea, Buldini, Barbara, Basso, Giuseppe, Bourquin, Jean-Pierre, Gaipa, Giuseppe, Brüggemann, Monika, Feuerstein, Tamar, Maurer-Granofszky, Margarita, Panzer-Grümayer, Renate, Trka, Jan, Mann, Georg, Haas, Oskar A, Hrusak, Ondrej, Dworzak, Michael N, and Strehl, Sabine

Published
2019

12. CD371 cell surface expression: a unique feature of DUX4-rearranged acute lymphoblastic leukemia

Author

Schinnerl, Dagmar, primary, Mejstrikova, Ester, additional, Schumich, Angela, additional, Zaliova, Marketa, additional, Fortschegger, Klaus, additional, Nebral, Karin, additional, Attarbaschi, Andishe, additional, Fiser, Karel, additional, Kauer, Maximilian O., additional, Popitsch, Niko, additional, Haslinger, Sabrina, additional, Inthal, Andrea, additional, Buldini, Barbara, additional, Basso, Giuseppe, additional, Bourquin, Jean-Pierre, additional, Gaipa, Giuseppe, additional, Brüggemann, Monika, additional, Feuerstein, Tamar, additional, Maurer-Granofszky, Margarita, additional, Panzer-Grümayer, Renate, additional, Trka, Jan, additional, Mann, Georg, additional, Haas, Oskar A., additional, Hrusak, Ondrej, additional, Dworzak, Michael N., additional, and Strehl, Sabine, additional

Published
2019
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16. Secreted microvesicular miR-31 inhibits osteogenic differentiation of mesenchymal stem cells

Author

Weilner, Sylvia, Schraml, Elisabeth, Wieser, Matthias, Messner, Paul, Schneider, Karl, Wassermann, Klemens, Micutkova, Lucia, Fortschegger, Klaus, Maier, Andrea B, Westendorp, Rudi, Resch, Heinrich, Wolbank, Susanne, Redl, Heinz, Jansen-Dürr, Pidder, Pietschmann, Peter, Grillari-Voglauer, Regina, Grillari, Johannes, Weilner, Sylvia, Schraml, Elisabeth, Wieser, Matthias, Messner, Paul, Schneider, Karl, Wassermann, Klemens, Micutkova, Lucia, Fortschegger, Klaus, Maier, Andrea B, Westendorp, Rudi, Resch, Heinrich, Wolbank, Susanne, Redl, Heinz, Jansen-Dürr, Pidder, Pietschmann, Peter, Grillari-Voglauer, Regina, and Grillari, Johannes

Abstract

Damage to cells and tissues is one of the driving forces of aging and age-related diseases. Various repair systems are in place to counteract this functional decline. In particular, the property of adult stem cells to self-renew and differentiate is essential for tissue homeostasis and regeneration. However, their functionality declines with age (Rando, 2006). One organ that is notably affected by the reduced differentiation capacity of stem cells with age is the skeleton. Here, we found that circulating microvesicles impact on the osteogenic differentiation capacity of mesenchymal stem cells in a donor-age-dependent way. While searching for factors mediating the inhibitory effect of elderly derived microvesicles on osteogenesis, we identified miR-31 as a crucial component. We demonstrated that miR-31 is present at elevated levels in the plasma of elderly and of osteoporosis patients. As a potential source of its secretion, we identified senescent endothelial cells, which are known to increase during aging in vivo (Erusalimsky, 2009). Endothelial miR-31 is secreted within senescent cell-derived microvesicles and taken up by mesenchymal stem cells where it inhibits osteogenic differentiation by knocking down its target Frizzled-3. Therefore, we suggest that microvesicular miR-31 in the plasma of elderly might play a role in the pathogenesis of age-related impaired bone formation and that miR-31 might be a valuable plasma-based biomarker for aging and for a systemic environment that does not favor cell-based therapies whenever osteogenesis is a limiting factor.

Published
2016

17. Secreted microvesicular miR-31 inhibits osteogenic differentiation of mesenchymal stem cells

Author

Weilner, Sylvia, primary, Schraml, Elisabeth, additional, Wieser, Matthias, additional, Messner, Paul, additional, Schneider, Karl, additional, Wassermann, Klemens, additional, Micutkova, Lucia, additional, Fortschegger, Klaus, additional, Maier, Andrea B., additional, Westendorp, Rudi, additional, Resch, Heinrich, additional, Wolbank, Susanne, additional, Redl, Heinz, additional, Jansen-Dürr, Pidder, additional, Pietschmann, Peter, additional, Grillari-Voglauer, Regina, additional, and Grillari, Johannes, additional

Published
2016
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18. Aging Cell / miR-17, miR-19b, miR-20a, and miR-106a are down-regulated in human aging

Author

Hackl, Matthias, Brunner, Stefan, Fortschegger, Klaus, Schreiner, Carina, Micutkova, Lucia, Mück, Christoph, Laschober, Gerhard T., Lepperdinger, Günter, Sampson, Natalie, Berger, Peter, Herndler-Brandstetter, Dietmar, Wieser, Matthias, Kühnel, Harald, Strasser, Alois, and Rinnerthaler, Mark

Abstract

Aging is a multifactorial process where deterioration of body functions is driven by stochastic damage while counteracted by distinct genetically encoded repair systems. To better understand the genetic component of aging, many studies have addressed the gene and protein expression profiles of various aging model systems engaging different organisms from yeast to human. The recently identified small non-coding miRNAs are potent post-transcriptional regulators that can modify the expression of up to several hundred target genes per single miRNA, similar to transcription factors. Increasing evidence shows that miRNAs contribute to the regulation of most if not all important physiological processes, including aging. However, so far the contribution of miRNAs to age-related and senescence-related changes in gene expression remains elusive. To address this question, we have selected four replicative cell aging models including endothelial cells, replicated CD8(+) T cells, renal proximal tubular epithelial cells, and skin fibroblasts. Further included were three organismal aging models including foreskin, mesenchymal stem cells, and CD8(+) T cell populations from old and young donors. Using locked nucleic acid-based miRNA microarrays, we identified four commonly regulated miRNAs, miR-17 down-regulated in all seven; miR-19b and miR-20a, down-regulated in six models; and miR-106a down-regulated in five models. Decrease in these miRNAs correlated with increased transcript levels of some established target genes, especially the cdk inhibitor p21/CDKN1A. These results establish miRNAs as novel markers of cell aging in humans. (VLID)2205399

Published
2010

20. Levels of circulating vesicular microRNA-31 increase with age as well as in the case of osteoporosis and inhibit osteogenic differentiation capacity of mesenchymal stem cells

Author

Weilner, Sylvia, primary, Schraml, Elisabeth, additional, Wassermann, Klemens, additional, Wieser, Matthias, additional, Messner, Paul, additional, Schneider, Karl, additional, Micutkova, Lucia, additional, Fortschegger, Klaus, additional, Maier, Andrea B., additional, Westendorp, Rudi, additional, Resch, Heinrich, additional, Wolbank, Susanne, additional, Redl, Heinz, additional, Jansen-Durr, Pidder, additional, Pietschmann, Peter, additional, Grillari-Voglauer, Regina, additional, and Grillari, Johannes, additional

Published
2014
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22. High levels of oncomi R ‐21 contribute to the senescence‐induced growth arrest in normal human cells and its knock‐down increases the replicative lifespan

Author

Dellago, Hanna, primary, Preschitz‐Kammerhofer, Barbara, additional, Terlecki‐Zaniewicz, Lucia, additional, Schreiner, Carina, additional, Fortschegger, Klaus, additional, Chang, Martina W.‐F., additional, Hackl, Matthias, additional, Monteforte, Rossella, additional, Kühnel, Harald, additional, Schosserer, Markus, additional, Gruber, Florian, additional, Tschachler, Erwin, additional, Scheideler, Marcel, additional, Grillari‐Voglauer, Regina, additional, Grillari, Johannes, additional, and Wieser, Matthias, additional

Published
2013
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23. Exo70, a subunit of the exocyst complex, interacts with SNEVhPrp19/hPso4 and is involved in pre-mRNA splicing

Author

Dellago, Hanna, primary, Löscher, Marlies, additional, Ajuh, Paul, additional, Ryder, Ursula, additional, Kaisermayer, Christian, additional, Grillari-Voglauer, Regina, additional, Fortschegger, Klaus, additional, Gross, Stefan, additional, Gstraunthaler, Anna, additional, Borth, Nicole, additional, Eisenhaber, Frank, additional, Lamond, Angus I., additional, and Grillari, Johannes, additional

Published
2011
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28. Blom7α Is a Novel Heterogeneous Nuclear Ribonucleoprotein K Homology Domain Protein Involved in Pre-mRNA Splicing That Interacts with SNEVPrp19-Pso4

Author

Grillari, Johannes, primary, Löscher, Marlies, additional, Denegri, Marco, additional, Lee, Kiseok, additional, Fortschegger, Klaus, additional, Eisenhaber, Frank, additional, Ajuh, Paul, additional, Lamond, Angus I., additional, Katinger, Hermann, additional, and Grillari-Voglauer, Regina, additional

Published
2009
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31. Interaction of U-box E3 ligase SNEV with PSMB4, the β7 subunit of the 20 S proteasome

Author

LÖSCHER, Marlies, primary, FORTSCHEGGER, Klaus, additional, RITTER, Gustav, additional, WOSTRY, Martina, additional, VOGLAUER, Regina, additional, SCHMID, Johannes A., additional, WATTERS, Steven, additional, RIVETT, A. Jennifer, additional, AJUH, Paul, additional, LAMOND, Angus I., additional, KATINGER, Hermann, additional, and GRILLARI, Johannes, additional

Published
2005
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32. Analysis of Alterations in Gene Expression after Amplification of Recombinant Genes in CHO Cells.

Author

Bernard, A., Griffiths, B., Noé, W., Wurm, F., Hohenwarter, Otmar, Grillari, Johannes, Fortschegger, Klaus, Grabherr, Reingard M., and Katinger, Hermann

Abstract

Dihydrofolate reductase based amplification of recombinant genes using increasing concentrations of methotrexate is a common method to establish CHO cell lines which secrete high amounts of the desired protein. We have investigated alterations in gene expression which occur beside amplification of the recombinant genes, because we wanted to define genes which are up- or downregulated in a cell line that shows highsecretion rates. For this purpose we have used the suppression hybridization method (SSH) to create a cDNA library which is enriched for differentially expressed sequences in the original and a recombinant antibody producing CHO cell line. Differential expression was confirmed by Northern Blotting and "Northern ELISA". In addition to the expected recombinant genes we have identified 5 genes which are upregulated in the recombinant cell line. One sequence has not been found in existing data bases, the others revealed to be genes involved in protein synthesis and regulation of transcription. Beside an improved characterization of altered gene expression in a recombinant CHO cell line the results prove the high efficiency of the SSH technique for abundant as well as for low copy number mRNAs. [ABSTRACT FROM AUTHOR]

Published
2000
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33. BIom7α Is a Novel Heterogeneous Nuclear Ribonucleoprotein K Homology Domain Protein Involved in Pre-mRNA Splicing That Interacts with SNEVPrp19-o4.

Author

Grillari, Johannes, Läscher, Marlies, Denegri, Marco, Kiseok Lee, Fortschegger, Klaus, Eisenhaber, Frank, Ajuh, Paul, Lamond, Angus I., Katinger, Hermann, and Grillari-Voglauer, Regina

Subjects
*NUCLEOPROTEINS, *INTRONS, *RNA splicing, *HOMOLOGY (Biology), *CATALYSIS
Abstract

The removal of introns from pre-mRNA is performed by the spliceosome that stepwise assembles on the pre-mRNA before performing two catalytic steps. The spliceosome-associated CDC5L-SNEVPrp19Pso4 complex is implicated in activation of the second catalytic step of pre-mRNA splicing, and one of its members, SNEVPrp19Pso4, is also implicated in spliceosome assembly. To identify interaction partners of SNEVPrp19-Pso4, we have performed yeast two-hybrid screenings. Among the putative binding partners was a so far uncharacterized protein carrying two heterogeneous nuclear ribonucleoprotein K homology domains that we termed Blom7α. Blom7α is expressed in all tissues tested, and at least three splice variants exist. After confirming direct and physical interaction of SNEV and Blom7α, we investigated if it plays a functional role during pre-mRNA splicing. Indeed, Blom7α co-localizes and co-precipitates with splicing factors and pre-mRNA and is present in affinity-purified spliceosomes. More importantly, addition of Blom7α to HeLa nuclear extracts increased splicing activity in a dose-dependent manner. Furthermore, we tested if Blom7α influences splice site selection using two different minigene constructs. Indeed, both 5'- as well as 3'-site selection was altered upon Blom7α overexpression. Thus we suggest that Blom7α is a novel splicing factor of the K homology domain family that might be implicated in alternative splicing by helping to position the CDC5L-SNEVPrp19Pso4 complex at the splice sites. [ABSTRACT FROM AUTHOR]

Published
2009
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34. Haploinsufficiency of senescence evasion factor causes defects of hematopoietic stem cells functions.

Author

Schraml E, Voglauer R, Fortschegger K, Sibilia M, Stelzer I, Grillari J, and Schauenstein K

Subjects
Animals, Blood Cells metabolism, Bone Marrow Cells metabolism, Cell Differentiation genetics, Cell Proliferation, Cells, Cultured, Female, Hematopoietic Stem Cells metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Nuclear Matrix-Associated Proteins metabolism, RNA Splicing Factors, Allelic Imbalance physiology, Hematopoietic Stem Cells physiology, Nuclear Matrix-Associated Proteins genetics
Abstract

The quality of hematopoietic stem cells (HSCs) is essentially defined by two characteristics, i.e., multilineage differentiation and self-renewal capacity. Thus, it is of high priority to clarify mechanisms that regulate these functions and to understand them at the molecular level. In the present study, we investigated the role of senescence evasion factor (synonymously hPrp19,hPSO4,hNMP200: SNEV), a multifunctional protein involved in pre-mRNA splicing, regulation of replicative life span, and DNA repair. Here we report that murine SNEV mRNA expression is high in lineage-depleted (Lin(-)) precursor cells of the bone marrow immediately after isolation as compared to fully differentiated peripheral blood lymphocytes (PBLs). Furthermore, the progenitor cell subset with highest colony-forming ability and self-renewal capacity (Lin(-), Sca-1(+)) showed also the highest SNEV expression. To test if the observed differences in SNEV mRNA levels cause stem cell defects, Lin(-) cells derived from heterozygous SNEV knockout mice were tested for primary as well as secondary colony-forming potential as a measure of self-renewal capacity. Interestingly, both, primary and secondary colonies were significantly less formed from SNEV(+/-) cells, a defect that was rescued by ectopic SNEV expression. Similarly, bone marrow cells derived from the short-lived Senescence-Accelerated-Mouse-Prone (SAMP8) model showed similar differences in comparison to the aging-resistant (SAMR1) control strain. These data suggest that the expression of SNEV is closely associated with the growth of murine HSCs and determines the proliferative and repopulating capacity of phenotypically defined HSC subsets.

Published
2008
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35. Interaction of U-box E3 ligase SNEV with PSMB4, the beta7 subunit of the 20 S proteasome.

Author

Löscher M, Fortschegger K, Ritter G, Wostry M, Voglauer R, Schmid JA, Watters S, Rivett AJ, Ajuh P, Lamond AI, Katinger H, and Grillari J

Subjects
Amino Acid Sequence, Animals, Binding Sites, Caenorhabditis elegans, Carrier Proteins chemistry, Cell Line, Conserved Sequence, Cysteine Endopeptidases physiology, DNA Repair Enzymes, Evolution, Molecular, Humans, Molecular Sequence Data, Nuclear Proteins, Proteasome Endopeptidase Complex chemistry, Protein Binding, Protein Conformation, RNA Splicing Factors, Sequence Homology, Amino Acid, Signal Transduction, Ubiquitin-Protein Ligases physiology, Cysteine Endopeptidases chemistry, Ubiquitin-Protein Ligases chemistry
Abstract

Recognition of specific substrates for degradation by the ubiquitin-proteasome pathway is ensured by a cascade of ubiquitin transferases E1, E2 and E3. The mechanism by which the target proteins are transported to the proteasome is not clear, but two yeast E3s and one mammalian E3 ligase seem to be involved in the delivery of targets to the proteasome, by escorting them and by binding to the 19 S regulatory particle of the proteasome. In the present study, we show that SNEV (senescence evasion factor), a protein with in vitro E3 ligase activity, which is also involved in DNA repair and splicing, associates with the proteasome by directly binding to the beta7 subunit of the 20 S proteasome. Upon inhibition of proteasome activity, SNEV does not accumulate within the cells although its co-localization with the proteasome increases significantly. Since immunofluorescence microscopy also shows increased co-localization of SNEV with ubiquitin after proteasome inhibition, without SNEV being ubiquitinated by itself, we suggest that SNEV shows E3 ligase activity not only in vitro but also in vivo and escorts its substrate to the proteasome. Since the yeast homologue of SNEV, Prp19, also interacts with the yeast beta7 subunit of the proteasome, this mechanism seems to be conserved during evolution. Therefore these results support the hypothesis that E3 ligases might generally be involved in substrate transport to the proteasome. Additionally, our results provide the first evidence for a physical link between components of the ubiquitin-proteasome system and the spliceosome.

Published
2005
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