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24 results on '"Hannus, Michael"'

1. Komplexe siRNA-Pools erzeugen optimales Gen-Silencing.

Author

Walsh, Andrew, Wobedo, Kevin, Burbach, Monika, Hannus, Michael, and Meister, Gunter

Abstract

Differences in the silencing efficiency of siRNAs for the same target gene affect the interpretability of RNAi experiments. The best way to ensure consistent and optimal gene silencing is to use a complex pool of siRNAs (siPOOLs). [ABSTRACT FROM AUTHOR]

Published
2024
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6. Argosomes: a potential vehicle for the spread of morphogens through epithelia

Author

Greco, Valentina, Hannus, Michael, and Eaton, Suzanne

Subjects
Drosophila -- Research, Membranes (Biology) -- Research, Morphogenesis -- Physiological aspects, Tissues -- Growth, Biological sciences
Abstract

Basolaterla membrane-derived argosomes are produced by several regions of the Drosophila imaginal disc epithelium, which eventually settle in endosomes. Data indicate that argosomes spread Wingless morphogen proteins in vivo.

Published
2001

7. High-Throughput RNA Interference Strategies for Target Discovery and Validation by Using Synthetic Short Interfering RNAs: Functional Genomics Investigations of Biological Pathways

Author

Sachse, Christoph, primary, Krausz, Eberhard, additional, Krönke, Andrea, additional, Hannus, Michael, additional, Walsh, Andrew, additional, Grabner, Anne, additional, Ovcharenko, Dmitriy, additional, Dorris, David, additional, Trudel, Claude, additional, Sönnichsen, Birte, additional, and Echeverri, Christophe J., additional

Published
2005
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9. Assessing gene function with siRNA libraries: Kinases affecting cell proliferation and mitotic index

Author

Kroenke, Andrea, Grabner, Anne, Hannus, Michael, Sachse, Christoph, Walsh, Andrew, Echeverri, Christophe, and Latham, Kathy

Subjects
Pharmaceuticals and cosmetics industries, Science and technology
Abstract

Sets of short interfering RNAs (siRNAs) focused on a specific gene class (siRNA libraries) have the capacity to greatly increase the pace of pathway analysis and functional genomics. In the [...]

Published
2004

10. Drug Screen Targeted at Plasmodium Liver Stages Identifies a Potent Multistage Antimalarial Drug

Author

da Cruz, Filipa P., Martin, Cécilie, Buchholz, Kathrin, Lafuente-Monasterio, Maria J., Rodrigues, Tiago, Sönnichsen, Birte, Moreira, Rui, Gamo, Francisco-Javier, Marti, Matthias, Mota, Maria M., Hannus, Michael, Prudêncio, Miguel, da Cruz, Filipa P., Martin, Cécilie, Buchholz, Kathrin, Lafuente-Monasterio, Maria J., Rodrigues, Tiago, Sönnichsen, Birte, Moreira, Rui, Gamo, Francisco-Javier, Marti, Matthias, Mota, Maria M., Hannus, Michael, and Prudêncio, Miguel

Abstract

Plasmodium parasites undergo a clinically silent and obligatory developmental phase in the host's liver cells before they are able to infect erythrocytes and cause malaria symptoms. To overcome the scarcity of compounds targeting the liver stage of malaria, we screened a library of 1037 existing drugs for their ability to inhibit Plasmodium hepatic development. Decoquinate emerged as the strongest inhibitor of Plasmodium liver stages, both in vitro and in vivo. Furthermore, decoquinate kills the parasite's replicative blood stages and is active against developing gametocytes, the forms responsible for transmission. The drug acts by selectively and specifically inhibiting the parasite's mitochondrial bc1 complex, with little cross-resistance with the antimalarial drug atovaquone. Oral administration of a single dose of decoquinate effectively prevents the appearance of disease, warranting its exploitation as a potent antimalarial compound

Published
2017

12. siRNA screen identifies QPCT as a druggable target for Huntington's disease.

Author

Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Jimenez-Sanchez, Maria, Lam, Wun, Hannus, Michael, Sonnichsen, Birte, Imarisio, Sara, Fleming, Angeleen, Tarditi, Alessia, Menzies, Fiona, Ed Dami, Teresa, Xu, Catherine, Gonzalez-Couto, Eduardo, Lazzeroni, Giulia, Heitz, Freddy, Diamanti, Daniela, Massai, Luisa, Satagopam, Venkata, Marconi, Guido, Caramelli, Chiara, Nencini, Arianna, Andreini, Matteo, Sardone, Gian Luca, Caradonna, Nicola P., Porcari, Valentina, Scali, Carla, Schneider, Reinhard, Pollio, Giuseppe, O'Kane, Cahir J., Caricasole, Andrea, Rubinsztein, David C., Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) [research center], Jimenez-Sanchez, Maria, Lam, Wun, Hannus, Michael, Sonnichsen, Birte, Imarisio, Sara, Fleming, Angeleen, Tarditi, Alessia, Menzies, Fiona, Ed Dami, Teresa, Xu, Catherine, Gonzalez-Couto, Eduardo, Lazzeroni, Giulia, Heitz, Freddy, Diamanti, Daniela, Massai, Luisa, Satagopam, Venkata, Marconi, Guido, Caramelli, Chiara, Nencini, Arianna, Andreini, Matteo, Sardone, Gian Luca, Caradonna, Nicola P., Porcari, Valentina, Scali, Carla, Schneider, Reinhard, Pollio, Giuseppe, O'Kane, Cahir J., Caricasole, Andrea, and Rubinsztein, David C.

Abstract

Huntington's disease (HD) is a currently incurable neurodegenerative condition caused by an abnormally expanded polyglutamine tract in huntingtin (HTT). We identified new modifiers of mutant HTT toxicity by performing a large-scale 'druggable genome' siRNA screen in human cultured cells, followed by hit validation in Drosophila. We focused on glutaminyl cyclase (QPCT), which had one of the strongest effects on mutant HTT-induced toxicity and aggregation in the cell-based siRNA screen and also rescued these phenotypes in Drosophila. We found that QPCT inhibition induced the levels of the molecular chaperone alphaB-crystallin and reduced the aggregation of diverse proteins. We generated new QPCT inhibitors using in silico methods followed by in vitro screening, which rescued the HD-related phenotypes in cell, Drosophila and zebrafish HD models. Our data reveal a new HD druggable target affecting mutant HTT aggregation and provide proof of principle for a discovery pipeline from druggable genome screen to drug development.

Published
2015

13. siRNA screen identifies QPCT as a druggable target for Huntington's disease

Author

Jimenez-Sanchez, Maria, primary, Lam, Wun, additional, Hannus, Michael, additional, Sönnichsen, Birte, additional, Imarisio, Sara, additional, Fleming, Angeleen, additional, Tarditi, Alessia, additional, Menzies, Fiona, additional, Ed Dami, Teresa, additional, Xu, Catherine, additional, Gonzalez-Couto, Eduardo, additional, Lazzeroni, Giulia, additional, Heitz, Freddy, additional, Diamanti, Daniela, additional, Massai, Luisa, additional, Satagopam, Venkata P, additional, Marconi, Guido, additional, Caramelli, Chiara, additional, Nencini, Arianna, additional, Andreini, Matteo, additional, Sardone, Gian Luca, additional, Caradonna, Nicola P, additional, Porcari, Valentina, additional, Scali, Carla, additional, Schneider, Reinhard, additional, Pollio, Giuseppe, additional, O'Kane, Cahir J, additional, Caricasole, Andrea, additional, and Rubinsztein, David C, additional

Published
2015
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14. Evaluation of Activity and Combination Strategies with the Microtubule-Targeting Drug Sagopilone in Breast Cancer Cell Lines

Author

Eschenbrenner, Julia, primary, Winsel, Sebastian, additional, Hammer, Stefanie, additional, Sommer, Anette, additional, Mittelstaedt, Kevin, additional, Drosch, Michael, additional, Klar, Ulrich, additional, Sachse, Christoph, additional, Hannus, Michael, additional, Seidel, Monika, additional, Weiss, Bertram, additional, Merz, Claudia, additional, Siemeister, Gerhard, additional, and Hoffmann, Jens, additional

Published
2011
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15. Kinome-Wide RNAi Screen Implicates at Least 5 Host Hepatocyte Kinases in Plasmodium Sporozoite Infection

Author

Prudêncio, Miguel, primary, Rodrigues, Cristina D., additional, Hannus, Michael, additional, Martin, Cécilie, additional, Real, Eliana, additional, Gonçalves, Lígia A., additional, Carret, Céline, additional, Dorkin, Robert, additional, Röhl, Ingo, additional, Jahn-Hoffmann, Kerstin, additional, Luty, Adrian J. F., additional, Sauerwein, Robert, additional, Echeverri, Christophe J., additional, and Mota, Maria M., additional

Published
2008
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16. Host Scavenger Receptor SR-BI Plays a Dual Role in the Establishment of Malaria Parasite Liver Infection

Author

Rodrigues, Cristina D., primary, Hannus, Michael, additional, Prudêncio, Miguel, additional, Martin, Cécilie, additional, Gonçalves, Lígia A., additional, Portugal, Sílvia, additional, Epiphanio, Sabrina, additional, Akinc, Akin, additional, Hadwiger, Philipp, additional, Jahn-Hofmann, Kerstin, additional, Röhl, Ingo, additional, van Gemert, Geert-Jan, additional, Franetich, Jean-François, additional, Luty, Adrian J.F., additional, Sauerwein, Robert, additional, Mazier, Dominique, additional, Koteliansky, Victor, additional, Vornlocher, Hans-Peter, additional, Echeverri, Christophe J., additional, and Mota, Maria M., additional

Published
2008
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17. Exploring the Full Power of Combining High Throughput RNAi with High Content Readouts: From Target Discovery Screens to Drug Modifier Studies

Author

Sachse, Christoph, primary, Weiss‐Haljiti, Cornelia, additional, Holz, Christian, additional, Regener, Kathrin, additional, Halley, Francoise, additional, Hannus, Michael, additional, Frenzel, Corina, additional, Kluge, Sindy, additional, Hewitson, Mark, additional, Bader, Benjamin, additional, Burd, Amy, additional, Perkins, Louise, additional, Szewczak, Alexander, additional, Prechtl, Stefan, additional, Merz, Claudia, additional, Rae, Peter, additional, Mumberg, Dominik, additional, and Echeverri, Christophe J., additional

Published
2007
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19. Argosomes

Author

Greco, Valentina, primary, Hannus, Michael, additional, and Eaton, Suzanne, additional

Published
2001
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21. Argosomes A Potential Vehicle for the Spread of Morphogens through Epithelia

Author

Greco, Valentina, Hannus, Michael, and Eaton, Suzanne

Subjects
animal structures, fungi, embryonic structures
Abstract

The formation of morphogen gradients is essential for tissue patterning. Morphogens are released from producing cells and spread through adjacent tissue; paradoxically, however, many morphogens, including Wingless, associate tightly with the cell membrane. Here, we describe a novel cell biological mechanism that disperses membrane fragments over large distances through the Drosophila imaginal disc epithelium. We call these membrane exovesicles argosomes. Argosomes are derived from basolateral membranes and are produced by many different regions of the disc. They travel through adjacent tissue where they are found predominantly in endosomes. Wingless protein colocalizes with argosomes derived from Wingless-producing cells. The properties of argosomes are consistent with their being a vehicle for the spread of Wingless protein.

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22. siRNA screen identifies QPCT as a druggable target for Huntington's disease

Author

Jimenez-Sanchez, Maria, Lam, Wun, Hannus, Michael, Sönnichsen, Birte, Imarisio, Sara, Fleming, Angeleen, Tarditi, Alessia, Menzies, Fiona, Dami, Teresa Ed, Xu, Catherine, Gonzalez-Couto, Eduardo, Lazzeroni, Giulia, Heitz, Freddy, Diamanti, Daniela, Massai, Luisa, Satagopam, Venkata P, Marconi, Guido, Caramelli, Chiara, Nencini, Arianna, Andreini, Matteo, Sardone, Gian Luca, Caradonna, Nicola P, Porcari, Valentina, Scali, Carla, Schneider, Reinhard, Pollio, Giuseppe, O'Kane, Cahir J, Caricasole, Andrea, and Rubinsztein, David C

Subjects
Neurons, congenital, hereditary, and neonatal diseases and abnormalities, Huntingtin Protein, Green Fluorescent Proteins, Drug Evaluation, Preclinical, Computational Biology, alpha-Crystallin B Chain, Nerve Tissue Proteins, Aminoacyltransferases, 3. Good health, Mice, Inbred C57BL, Mice, Huntington Disease, mental disorders, Mutation, Animals, Humans, Drosophila, Enzyme Inhibitors, RNA, Small Interfering, Cells, Cultured, Zebrafish
Abstract

Huntington's disease (HD) is a currently incurable neurodegenerative condition caused by an abnormally expanded polyglutamine tract in huntingtin (HTT). We identified new modifiers of mutant HTT toxicity by performing a large-scale 'druggable genome' siRNA screen in human cultured cells, followed by hit validation in Drosophila. We focused on glutaminyl cyclase (QPCT), which had one of the strongest effects on mutant HTT-induced toxicity and aggregation in the cell-based siRNA screen and also rescued these phenotypes in Drosophila. We found that QPCT inhibition induced the levels of the molecular chaperone αB-crystallin and reduced the aggregation of diverse proteins. We generated new QPCT inhibitors using in silico methods followed by in vitro screening, which rescued the HD-related phenotypes in cell, Drosophila and zebrafish HD models. Our data reveal a new HD druggable target affecting mutant HTT aggregation and provide proof of principle for a discovery pipeline from druggable genome screen to drug development.

23. Drug Screen Targeted at Plasmodium Liver Stages Identifies a Potent Multistage Antimalarial Drug

Author

da Cruz, Filipa P., Martin, Cecilie, Buchholz, Kathrin, Lafuente-Monasterio, Maria J., Rodrigues, Tiago, Sonnichsen, Birte, Moreira, Rui, Gamo, Francisco-Javier, Marti, Matthias, Mota, Maria M., Hannus, Michael, and Prudencio, Miguel

Subjects
education, health care economics and organizations, humanities, 3. Good health
Abstract

The Journal of Infectious Diseases, 205 (8), ISSN:0022-1899, ISSN:1537-6613

24. Drug Screen Targeted at Plasmodium Liver Stages Identifies a Potent Multistage Antimalarial Drug

Author

da Cruz, Filipa P., Martin, Cécilie, Buchholz, Kathrin, Lafuente-Monasterio, Maria J., Rodrigues, Tiago, Sönnichsen, Birte, Moreira, Rui, Gamo, Francisco-Javier, Marti, Matthias, Mota, Maria M., Hannus, Michael, Prudêncio, Miguel, da Cruz, Filipa P., Martin, Cécilie, Buchholz, Kathrin, Lafuente-Monasterio, Maria J., Rodrigues, Tiago, Sönnichsen, Birte, Moreira, Rui, Gamo, Francisco-Javier, Marti, Matthias, Mota, Maria M., Hannus, Michael, and Prudêncio, Miguel

Abstract

Plasmodium parasites undergo a clinically silent and obligatory developmental phase in the host's liver cells before they are able to infect erythrocytes and cause malaria symptoms. To overcome the scarcity of compounds targeting the liver stage of malaria, we screened a library of 1037 existing drugs for their ability to inhibit Plasmodium hepatic development. Decoquinate emerged as the strongest inhibitor of Plasmodium liver stages, both in vitro and in vivo. Furthermore, decoquinate kills the parasite's replicative blood stages and is active against developing gametocytes, the forms responsible for transmission. The drug acts by selectively and specifically inhibiting the parasite's mitochondrial bc1 complex, with little cross-resistance with the antimalarial drug atovaquone. Oral administration of a single dose of decoquinate effectively prevents the appearance of disease, warranting its exploitation as a potent antimalarial compound

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