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1. Biallelic MAD2L1BP (p31comet) mutation is associated with mosaic aneuploidy and juvenile granulosa cell tumors

Author

Abdel-Salam, Ghada M. H., primary, Hellmuth, Susanne, additional, Gradhand, Elise, additional, Käseberg, Stephan, additional, Winter, Jennifer, additional, Pabst, Ann-Sophie, additional, Eid, Maha M., additional, Thiele, Holger, additional, Nürnberg, Peter, additional, Budde, Birgit S., additional, Toliat, Mohammad Reza, additional, Brecht, Ines B., additional, Schroeder, Christopher, additional, Gschwind, Axel, additional, Ossowski, Stephan, additional, Häuser, Friederike, additional, Rossmann, Heidi, additional, Abdel-Hamid, Mohamed S., additional, Hegazy, Ibrahim, additional, Mohamed, Ahmed G., additional, Schneider, Dominik T., additional, Bertoli-Avella, Aida, additional, Bauer, Peter, additional, Pearring, Jillian N., additional, Pfundt, Rolph, additional, Hoischen, Alexander, additional, Gilissen, Christian, additional, Strand, Dennis, additional, Zechner, Ulrich, additional, Tashkandi, Soha A., additional, Faqeih, Eissa A., additional, Stemmann, Olaf, additional, Strand, Susanne, additional, and Bolz, Hanno J., additional

Published
2023
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4. Externalized histones fuel pulmonary fibrosis via a platelet-macrophage circuit of TGFβ1 and IL-27

Author

Riehl, Dennis R., primary, Sharma, Arjun, additional, Roewe, Julian, additional, Murke, Florian, additional, Ruppert, Clemens, additional, Eming, Sabine A., additional, Bopp, Tobias, additional, Kleinert, Hartmut, additional, Radsak, Markus P., additional, Colucci, Giuseppe, additional, Subramaniam, Saravanan, additional, Reinhardt, Christoph, additional, Giebel, Bernd, additional, Prinz, Immo, additional, Guenther, Andreas, additional, Strand, Dennis, additional, Gunzer, Matthias, additional, Waisman, Ari, additional, Ward, Peter A., additional, Ruf, Wolfram, additional, Schäfer, Katrin, additional, and Bosmann, Markus, additional

Published
2023
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7. Supplementary Methods and Materials from The Transcriptional Repressor ZEB1 Promotes Metastasis and Loss of Cell Polarity in Cancer

Author

Spaderna, Simone, primary, Schmalhofer, Otto, primary, Wahlbuhl, Mandy, primary, Dimmler, Arno, primary, Bauer, Katja, primary, Sultan, Aneesa, primary, Hlubek, Falk, primary, Jung, Andreas, primary, Strand, Dennis, primary, Eger, Andreas, primary, Kirchner, Thomas, primary, Behrens, Jürgen, primary, and Brabletz, Thomas, primary

Published
2023
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8. Supplementary Figure 3 from The Transcriptional Repressor ZEB1 Promotes Metastasis and Loss of Cell Polarity in Cancer

Author

Spaderna, Simone, primary, Schmalhofer, Otto, primary, Wahlbuhl, Mandy, primary, Dimmler, Arno, primary, Bauer, Katja, primary, Sultan, Aneesa, primary, Hlubek, Falk, primary, Jung, Andreas, primary, Strand, Dennis, primary, Eger, Andreas, primary, Kirchner, Thomas, primary, Behrens, Jürgen, primary, and Brabletz, Thomas, primary

Published
2023
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9. Supplementary Figure Legends 1-3 from The Transcriptional Repressor ZEB1 Promotes Metastasis and Loss of Cell Polarity in Cancer

Author

Spaderna, Simone, primary, Schmalhofer, Otto, primary, Wahlbuhl, Mandy, primary, Dimmler, Arno, primary, Bauer, Katja, primary, Sultan, Aneesa, primary, Hlubek, Falk, primary, Jung, Andreas, primary, Strand, Dennis, primary, Eger, Andreas, primary, Kirchner, Thomas, primary, Behrens, Jürgen, primary, and Brabletz, Thomas, primary

Published
2023
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10. Supplementary Figure 2 from The Transcriptional Repressor ZEB1 Promotes Metastasis and Loss of Cell Polarity in Cancer

Author

Spaderna, Simone, primary, Schmalhofer, Otto, primary, Wahlbuhl, Mandy, primary, Dimmler, Arno, primary, Bauer, Katja, primary, Sultan, Aneesa, primary, Hlubek, Falk, primary, Jung, Andreas, primary, Strand, Dennis, primary, Eger, Andreas, primary, Kirchner, Thomas, primary, Behrens, Jürgen, primary, and Brabletz, Thomas, primary

Published
2023
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12. Supplementary Figure 1 from The Transcriptional Repressor ZEB1 Promotes Metastasis and Loss of Cell Polarity in Cancer

Author

Spaderna, Simone, primary, Schmalhofer, Otto, primary, Wahlbuhl, Mandy, primary, Dimmler, Arno, primary, Bauer, Katja, primary, Sultan, Aneesa, primary, Hlubek, Falk, primary, Jung, Andreas, primary, Strand, Dennis, primary, Eger, Andreas, primary, Kirchner, Thomas, primary, Behrens, Jürgen, primary, and Brabletz, Thomas, primary

Published
2023
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23. Lipid presentation by the protein C receptor links coagulation with autoimmunity

Author

Müller-Calleja, Nadine, primary, Hollerbach, Anne, additional, Royce, Jennifer, additional, Ritter, Svenja, additional, Pedrosa, Denise, additional, Madhusudhan, Thati, additional, Teifel, Sina, additional, Meineck, Myriam, additional, Häuser, Friederike, additional, Canisius, Antje, additional, Nguyen, T. Son, additional, Braun, Johannes, additional, Bruns, Kai, additional, Etzold, Anna, additional, Zechner, Ulrich, additional, Strand, Susanne, additional, Radsak, Markus, additional, Strand, Dennis, additional, Gu, Jian-Ming, additional, Weinmann-Menke, Julia, additional, Esmon, Charles T., additional, Teyton, Luc, additional, Lackner, Karl J., additional, and Ruf, Wolfram, additional

Published
2021
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36. 6-Mercaptopurine and 9-(2-Phosphonyl- Methoxyethyl) Adenine (PMEA) Transport Altered by Two Missense Mutations in the Drug Transporter Gene ABCC4

Author

Janke, Daniel, Mehralivand, Sherif, Strand, Dennis, Gödtel-Armbrust, Ute, Habermeier, Alice, Gradhand, Ulrike, Fischer, Christine, Toliat, Mohammad R., Fritz, Peter, Zanger, Ulrich M., Schwab, Matthias, Fromm, Martin F., Nürnberg, Peter, Wojnowski, Leszek, Closs, Ellen I., Lang, Thomas, and Ferec, Claude

Published
2008
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42. Abstract 267: Targeting the alt-NHEJ DNA repair pathway selectively sensitizes KRAS-mutant cancer cells to chemotherapy

Author

Haehnel, Patricia S., primary, Swoboda, Sarah, additional, Lehmann, Nadine, additional, Rosigkeit, Sebastian, additional, Gothe, Hernike, additional, Sasca, Danial I., additional, Strand, Dennis, additional, Theobald, Matthias, additional, Roukos, Vassilis, additional, Bockamp, Ernesto, additional, and Kindler, Thomas, additional

Published
2019
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43. Ginkgo biloba induces different gene expression signatures and oncogenic pathways in malignant and non-malignant cells of the liver

Author

Czauderna, Carolin, primary, Palestino-Dominguez, Mayrel, additional, Castven, Darko, additional, Becker, Diana, additional, Zanon-Rodriguez, Luis, additional, Hajduk, Jovana, additional, Mahn, Friederike L., additional, Herr, Monika, additional, Strand, Dennis, additional, Strand, Susanne, additional, Heilmann-Heimbach, Stefanie, additional, Gomez-Quiroz, Luis E., additional, Wörns, Marcus A., additional, Galle, Peter R., additional, and Marquardt, Jens U., additional

Published
2018
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44. The lethal giant larvae tumour suppressor mutation requires dMyc oncoprotein to promote clonal malignancy

Author

Bellosta Paola, Grzeschik Nicola A, Pession Andrea, Garoia Flavio, Ziosi Marcello, Froldi Francesca, Strand Dennis, Richardson Helena E, Pession Annalisa, and Grifoni Daniela

Subjects
Biology (General), QH301-705.5
Abstract

Abstract Background Neoplastic overgrowth depends on the cooperation of several mutations ultimately leading to major rearrangements in cellular behaviour. Precancerous cells are often removed by cell death from normal tissues in the early steps of the tumourigenic process, but the molecules responsible for such a fundamental safeguard process remain in part elusive. With the aim to investigate the molecular crosstalk occurring between precancerous and normal cells in vivo, we took advantage of the clonal analysis methods that are available in Drosophila for studying the phenotypes due to lethal giant larvae (lgl) neoplastic mutation induced in different backgrounds and tissues. Results We observed that lgl mutant cells growing in wild-type imaginal wing discs show poor viability and are eliminated by Jun N-terminal Kinase (JNK)-dependent cell death. Furthermore, they express very low levels of dMyc oncoprotein compared with those found in the surrounding normal tissue. Evidence that this is a cause of lgl mutant cells elimination was obtained by increasing dMyc levels in lgl mutant clones: their overgrowth potential was indeed re-established, with mutant cells overwhelming the neighbouring tissue and forming tumourous masses displaying several cancer hallmarks. Moreover, when lgl mutant clones were induced in backgrounds of slow-dividing cells, they upregulated dMyc, lost apical-basal cell polarity and were able to overgrow. Those phenotypes were abolished by reducing dMyc levels in the mutant clones, thereby confirming its key role in lgl-induced tumourigenesis. Furthermore, we show that the eiger-dependent Intrinsic Tumour Suppressor pathway plays only a minor role in eliminating lgl mutant cells in the wing pouch; lgl-/- clonal death in this region is instead driven mainly by dMyc-induced Cell Competition. Conclusions Our results provide the first evidence that dMyc oncoprotein is required in lgl tumour suppressor mutant tissue to promote invasive overgrowth in larval and adult epithelial tissues. Moreover, we show that dMyc abundance inside versus outside the mutant clones plays a key role in driving neoplastic overgrowth.

Published
2010
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45. Autophagy interferes with human cytomegalovirus genome replication, morphogenesis, and progeny release.

Author

Zimmermann, Christine, Krämer, Nadine, Krauter, Steffi, Strand, Dennis, Sehn, Elisabeth, Wolfrum, Uwe, Freiwald, Anja, Butter, Falk, and Plachter, Bodo

Subjects
AUTOPHAGY, CYTOMEGALOVIRUSES, VIRAL genomes, VIRAL replication, MORPHOGENESIS
Abstract

Viral infections are often accompanied by the induction of autophagy as an intrinsic cellular defense mechanism. Herpesviruses have developed strategies to evade autophagic degradation and to manipulate autophagy of the host cells to their benefit. Here we addressed the role of macroautophagy/autophagy in human cytomegalovirus replication and for particle morphogenesis. We found that proteins of the autophagy machinery localize to cytoplasmic viral assembly compartments and enveloped virions in the cytoplasm. Surprisingly, the autophagy receptor SQSTM1/p62 was also found to colocalize with HCMV capsids in the nucleus of infected cells. This finding indicates that the autophagy machinery interacts with HCMV already at the early nuclear stages of particle morphogenesis. The membrane-bound form of LC3 and several autophagy receptors were packaged into extracellular HCMV virions. This suggested that autophagic membranes were included during secondary envelopment of HCMV virions. To further address the importance of autophagy in HCMV infection, we generated an HCMV mutant that expressed a dominant-negative version of the protease ATG4B (BAD-ATG4BC74A). The proteolytic activity of ATG4B is required for LC3 cleavage, priming it for membrane conjugation. Surprisingly, both genome replication and virus release were enhanced in cells infected with BAD-ATG4BC74A, compared to control strains. These results show that autophagy operates as an antiviral process during HCMV infection but is dispensable for secondary HCMV particle envelopment. Abbreviations: ATG: autophagy-related; BAC: bacterial artificial chromosome; BECN1: beclin 1; CPE: cytopathic effect; cVACs: cytoplasmic viral assembly compartments; d.p.i.: days post-infection; DB: dense body; EBV: Epstein-Barr virus; galK: galactokinase; HCMV: human cytomegalovirus; HFF: human foreskin fibroblasts; IE: immediate-early; IRS: internal repeat short; LC3: MAP1LC3A/B; m.o.i.; multiplicity of infection; MCP: major capsid protein; Pp: phosphoprotein; sCP/UL48a: smallest capsid protein; TRS: terminal repeat short; UL: unique long; US: unique short [ABSTRACT FROM AUTHOR]

Published
2021
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46. Inducible knockdown of procollagen I protects mice from liver fibrosis and leads to dysregulated matrix genes and attenuated inflammation

Author

Molokanova, Olena, primary, Schönig, Kai, additional, Weng, Shih-Yen, additional, Wang, Xiaoyu, additional, Bros, Matthias, additional, Diken, Mustafa, additional, Ohngemach, Svetlana, additional, Karsdal, Morten, additional, Strand, Dennis, additional, Nikolaev, Alexei, additional, Eshkind, Leonid, additional, and Schuppan, Detlef, additional

Published
2018
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48. Activation of silent mating type information regulation 2 homolog 1 by human chorionic gonadotropin exerts a therapeutic effect on hepatic injury and inflammation

Author

Steinmetz, Caroline, primary, Kashyap, Anubha, additional, Zhivkova, Nataliya, additional, Alizor, Henry, additional, Ernst, Isabell, additional, Gottfried‐Brand, Daniela, additional, Janssen, Henning, additional, Teufel, Andreas, additional, Schulze‐Bergkamen, Henning, additional, Lotz, Johannes, additional, Kuball, Jürgen, additional, Theobald, Matthias, additional, Heise, Michael, additional, Lang, Hauke, additional, Galle, Peter R., additional, Strand, Dennis, additional, and Strand, Susanne, additional

Published
2017
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49. Adverse genomic alterations and stemness features are induced by field cancerization in the microenvironment of hepatocellular carcinomas

Author

Castven, Darko, primary, Fischer, Michael, additional, Becker, Diana, additional, Heinrich, Stefan, additional, Andersen, Jesper B., additional, Strand, Dennis, additional, Sprinzl, Martin F., additional, Strand, Susanne, additional, Czauderna, Carolin, additional, Heilmann-Heimbach, Stefanie, additional, Roessler, Stephanie, additional, Weinmann, Arndt, additional, Wörns, Marcus A., additional, Thorgeirsson, Snorri S., additional, Galle, Peter R., additional, Matter, Matthias S., additional, Lang, Hauke, additional, and Marquardt, Jens U., additional

Published
2017
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50. Glycine-functionalized copper(ii) hydroxide nanoparticles with high intrinsic superoxide dismutase activity

Author

Korschelt, Karsten, primary, Ragg, Ruben, additional, Metzger, Carmen S., additional, Kluenker, Martin, additional, Oster, Michael, additional, Barton, Bastian, additional, Panthöfer, Martin, additional, Strand, Dennis, additional, Kolb, Ute, additional, Mondeshki, Mihail, additional, Strand, Susanne, additional, Brieger, Jürgen, additional, Nawaz Tahir, M., additional, and Tremel, Wolfgang, additional

Published
2017
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